(2S-(2 alpha,3 beta,4 beta))-2-Carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid. Ascaricide obtained from the red alga Digenea simplex. It is a potent excitatory amino acid agonist at some types of excitatory amino acid receptors and has been used to discriminate among receptor types. Like many excitatory amino acid agonists it can cause neurotoxicity and has been used experimentally for that purpose.
Drugs that bind to and activate excitatory amino acid receptors.
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."
A class of ionotropic glutamate receptors characterized by their affinity for KAINIC ACID.
A prolonged seizure or seizures repeated frequently enough to prevent recovery between episodes occurring over a period of 20-30 minutes. The most common subtype is generalized tonic-clonic status epilepticus, a potentially fatal condition associated with neuronal injury and respiratory and metabolic dysfunction. Nonconvulsive forms include petit mal status and complex partial status, which may manifest as behavioral disturbances. Simple partial status epilepticus consists of persistent motor, sensory, or autonomic seizures that do not impair cognition (see also EPILEPSIA PARTIALIS CONTINUA). Subclinical status epilepticus generally refers to seizures occurring in an unresponsive or comatose individual in the absence of overt signs of seizure activity. (From N Engl J Med 1998 Apr 2;338(14):970-6; Neurologia 1997 Dec;12 Suppl 6:25-30)
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
Substances that act in the brain stem or spinal cord to produce tonic or clonic convulsions, often by removing normal inhibitory tone. They were formerly used to stimulate respiration or as antidotes to barbiturate overdose. They are now most commonly used as experimental tools.
A convulsant primarily used in experimental animals. It was formerly used to induce convulsions as a alternative to electroshock therapy.
An amino acid that, as the D-isomer, is the defining agonist for the NMDA receptor subtype of glutamate receptors (RECEPTORS, NMDA).
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.
The repeated weak excitation of brain structures, that progressively increases sensitivity to the same stimulation. Over time, this can lower the threshold required to trigger seizures.
A pharmaceutical agent that displays activity as a central nervous system and respiratory stimulant. It is considered a non-competitive GAMMA-AMINOBUTYRIC ACID antagonist. Pentylenetetrazole has been used experimentally to study seizure phenomenon and to identify pharmaceuticals that may control seizure susceptibility.
The lower portion of the BRAIN STEM. It is inferior to the PONS and anterior to the CEREBELLUM. Medulla oblongata serves as a relay station between the brain and the spinal cord, and contains centers for regulating respiratory, vasomotor, cardiac, and reflex activities.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
A localization-related (focal) form of epilepsy characterized by recurrent seizures that arise from foci within the temporal lobe, most commonly from its mesial aspect. A wide variety of psychic phenomena may be associated, including illusions, hallucinations, dyscognitive states, and affective experiences. The majority of complex partial seizures (see EPILEPSY, COMPLEX PARTIAL) originate from the temporal lobes. Temporal lobe seizures may be classified by etiology as cryptogenic, familial, or symptomatic (i.e., related to an identified disease process or lesion). (From Adams et al., Principles of Neurology, 6th ed, p321)
Cell surface receptors that bind signalling molecules released by neurons and convert these signals into intracellular changes influencing the behavior of cells. Neurotransmitter is used here in its most general sense, including not only messengers that act to regulate ion channels, but also those which act on second messenger systems and those which may act at a distance from their release sites. Included are receptors for neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not located at synapses.
Quinolinic acid is a physiologically occurring metabolite of the kynurenine pathway, involved in the metabolism of tryptophan, which functions as a neuroexcitatory agent and has been implicated in several neurological disorders, including Huntington's disease and HIV-associated dementia.
Nerve cells where transmission is mediated by NITRIC OXIDE.
A neurotoxic isoxazole (similar to KAINIC ACID and MUSCIMOL) found in AMANITA mushrooms. It causes motor depression, ataxia, and changes in mood, perceptions and feelings, and is a potent excitatory amino acid agonist.
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)
An inhibitor of the enzyme TYROSINE 3-MONOOXYGENASE, and consequently of the synthesis of catecholamines. It is used to control the symptoms of excessive sympathetic stimulation in patients with PHEOCHROMOCYTOMA. (Martindale, The Extra Pharmacopoeia, 30th ed)
Axons of certain cells in the DENTATE GYRUS. They project to the polymorphic layer of the dentate gyrus and to the proximal dendrites of PYRAMIDAL CELLS of the HIPPOCAMPUS. These mossy fibers should not be confused with mossy fibers that are cerebellar afferents (see NERVE FIBERS).
Cell-surface proteins that bind glutamate and trigger changes which influence the behavior of cells. Glutamate receptors include ionotropic receptors (AMPA, kainate, and N-methyl-D-aspartate receptors), which directly control ion channels, and metabotropic receptors which act through second messenger systems. Glutamate receptors are the most common mediators of fast excitatory synaptic transmission in the central nervous system. They have also been implicated in the mechanisms of memory and of many diseases.
The four cellular masses in the floor of the fourth ventricle giving rise to a widely dispersed special sensory system. Included is the superior, medial, inferior, and LATERAL VESTIBULAR NUCLEUS. (From Dorland, 27th ed)
Derivatives of GLUTAMIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the 2-aminopentanedioic acid structure.
Pyrrolidines are saturated, heterocyclic organic compounds containing a five-membered ring with four carbon atoms and one nitrogen atom (NRCH2CH2), commonly found as structural components in various alkaloids and used in the synthesis of pharmaceuticals and other organic materials.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
An agonist at two subsets of excitatory amino acid receptors, ionotropic receptors that directly control membrane channels and metabotropic receptors that indirectly mediate calcium mobilization from intracellular stores. The compound is obtained from the seeds and fruit of Quisqualis chinensis.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
Central gray matter surrounding the CEREBRAL AQUEDUCT in the MESENCEPHALON. Physiologically it is probably involved in RAGE reactions, the LORDOSIS REFLEX; FEEDING responses, bladder tonus, and pain.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
An IBOTENIC ACID homolog and glutamate agonist. The compound is the defining agonist for the AMPA subtype of glutamate receptors (RECEPTORS, AMPA). It has been used as a radionuclide imaging agent but is more commonly used as an experimental tool in cell biological studies.
A metabolite of tryptophan with a possible role in neurodegenerative disorders. Elevated CSF levels of quinolinic acid are correlated with the severity of neuropsychological deficits in patients who have AIDS.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
Drugs used to prevent SEIZURES or reduce their severity.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Endogenous amino acids released by neurons as excitatory neurotransmitters. Glutamic acid is the most common excitatory neurotransmitter in the brain. Aspartic acid has been regarded as an excitatory transmitter for many years, but the extent of its role as a transmitter is unclear.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
Involuntary rhythmical movements of the eyes in the normal person. These can be naturally occurring as in end-position (end-point, end-stage, or deviational) nystagmus or induced by the optokinetic drum (NYSTAGMUS, OPTOKINETIC), caloric test, or a rotating chair.
A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.
Increased levels of PROLACTIN in the BLOOD, which may be associated with AMENORRHEA and GALACTORRHEA. Relatively common etiologies include PROLACTINOMA, medication effect, KIDNEY FAILURE, granulomatous diseases of the PITUITARY GLAND, and disorders which interfere with the hypothalamic inhibition of prolactin release. Ectopic (non-pituitary) production of prolactin may also occur. (From Joynt, Clinical Neurology, 1992, Ch36, pp77-8)
The injection of very small amounts of fluid, often with the aid of a microscope and microsyringes.
Injections into the cerebral ventricles.
Recording of electric currents developed in the brain by means of electrodes applied to the scalp, to the surface of the brain, or placed within the substance of the brain.
GRAY MATTER situated above the GYRUS HIPPOCAMPI. It is composed of three layers. The molecular layer is continuous with the HIPPOCAMPUS in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called GRANULE CELLS, whose AXONS pass through the polymorphic layer ending on the DENDRITES of PYRAMIDAL CELLS in the hippocampus.
The front part of the hindbrain (RHOMBENCEPHALON) that lies between the MEDULLA and the midbrain (MESENCEPHALON) ventral to the cerebellum. It is composed of two parts, the dorsal and the ventral. The pons serves as a relay station for neural pathways between the CEREBELLUM to the CEREBRUM.
A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
The observable response an animal makes to any situation.
A potent excitatory amino acid antagonist with a preference for non-NMDA iontropic receptors. It is used primarily as a research tool.
A flavoprotein that reversibly oxidizes NADPH to NADP and a reduced acceptor. EC
Quinoxalines are heterocyclic organic compounds consisting of a benzene fused to a pyrazine ring, which have been studied for their potential antibacterial, antifungal, and anticancer properties.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
A set of forebrain structures common to all mammals that is defined functionally and anatomically. It is implicated in the higher integration of visceral, olfactory, and somatic information as well as homeostatic responses including fundamental survival behaviors (feeding, mating, emotion). For most authors, it includes the AMYGDALA; EPITHALAMUS; GYRUS CINGULI; hippocampal formation (see HIPPOCAMPUS); HYPOTHALAMUS; PARAHIPPOCAMPAL GYRUS; SEPTAL NUCLEI; anterior nuclear group of thalamus, and portions of the basal ganglia. (Parent, Carpenter's Human Neuroanatomy, 9th ed, p744; NeuroNames, http://rprcsgi.rprc.washington.edu/neuronames/index.html (September 2, 1998)).

In vivo intracellular analysis of granule cell axon reorganization in epileptic rats. (1/1468)

In vivo intracellular recording and labeling in kainate-induced epileptic rats was used to address questions about granule cell axon reorganization in temporal lobe epilepsy. Individually labeled granule cells were reconstructed three dimensionally and in their entirety. Compared with controls, granule cells in epileptic rats had longer average axon length per cell; the difference was significant in all strata of the dentate gyrus including the hilus. In epileptic rats, at least one-third of the granule cells extended an aberrant axon collateral into the molecular layer. Axon projections into the molecular layer had an average summed length of 1 mm per cell and spanned 600 microm of the septotemporal axis of the hippocampus-a distance within the normal span of granule cell axon collaterals. These findings in vivo confirm results from previous in vitro studies. Surprisingly, 12% of the granule cells in epileptic rats, and none in controls, extended a basal dendrite into the hilus, providing another route for recurrent excitation. Consistent with recurrent excitation, many granule cells (56%) in epileptic rats displayed a long-latency depolarization superimposed on a normal inhibitory postsynaptic potential. These findings demonstrate changes, occurring at the single-cell level after an epileptogenic hippocampal injury, that could result in novel, local, recurrent circuits.  (+info)

Preferential Zn2+ influx through Ca2+-permeable AMPA/kainate channels triggers prolonged mitochondrial superoxide production. (2/1468)

Synaptically released Zn2+ can enter and cause injury to postsynaptic neurons. Microfluorimetric studies using the Zn2+-sensitive probe, Newport green, examined levels of [Zn2+]i attained in cultured cortical neurons on exposure to N-methyl-D-asparte, kainate, or high K+ (to activate voltage-sensitive Ca2+ channels) in the presence of 300 microM Zn2+. Indicating particularly high permeability through Ca2+-permeable alpha-amino3-hydroxy-5-methyl-4-isoxazolepropionic-acid/kainate (Ca-A/K) channels, micromolar [Zn2+]i rises were observed only after kainate exposures and only in neurons expressing these channels [Ca-A/K(+) neurons]. Further studies using the oxidation-sensitive dye, hydroethidine, revealed Zn2+-dependent reactive oxygen species (ROS) generation that paralleled the [Zn2+]i rises, with rapid oxidation observed only in the case of Zn2+ entry through Ca-A/K channels. Indicating a mitochondrial source of this ROS generation, hydroethidine oxidation was inhibited by the mitochondrial electron transport blocker, rotenone. Additional evidence for a direct interaction between Zn2+ and mitochondria was provided by the observation that the Zn2+ entry through Ca-A/K channels triggered rapid mitochondrial depolarization, as assessed by using the potential-sensitive dye tetramethylrhodamine ethylester. Whereas Ca2+ influx through Ca-A/K channels also triggers ROS production, the [Zn2+]i rises and subsequent ROS production are of more prolonged duration.  (+info)

Glutamate-, kainate- and NMDA-evoked membrane currents in identified glial cells in rat spinal cord slice. (3/1468)

The effect of L-glutamate, kainate and N-methyl-D-aspartate (NMDA) on membrane currents of astrocytes, oligodendrocytes and their respective precursors was studied in acute spinal cord slices of rats between the ages of postnatal days 5 and 13 using the whole-cell patch-clamp technique. L-glutamate (10(-3) M), kainate (10(-3) M), and NMDA (2x10(-3) M) evoked inward currents in all glial cells. Kainate evoked larger currents in precursors than in astrocytes and oligodendrocytes, while NMDA induced larger currents in astrocytes and oligodendrocytes than in precursors. Kainate-evoked currents were blocked by the AMPA/kainate receptor antagonist CNQX (10(-4) M) and were, with the exception of the precursors, larger in dorsal than in ventral horns, as were NMDA-evoked currents. Currents evoked by NMDA were unaffected by CNQX and, in contrast to those seen in neurones, were not sensitive to Mg2+. In addition, they significantly decreased during development and were present when synaptic transmission was blocked in a Ca2+-free solution. NMDA-evoked currents were not abolished during the block of K+ inward currents in glial cells by Ba2+; thus they are unlikely to be mediated by an increase in extracellular K+ during neuronal activity. We provide evidence that spinal cord glial cells are sensitive to the application of L-glutamate, kainate and transiently, during postnatal development, to NMDA.  (+info)

The distribution of neurons expressing calcium-permeable AMPA receptors in the superficial laminae of the spinal cord dorsal horn. (4/1468)

The superficial dorsal horn is a major site of termination of nociceptive primary afferents. Fast excitatory synaptic transmission in this region is mediated mainly by release of glutamate onto postsynaptic AMPA and NMDA receptors. NMDA receptors are known to be Ca2+-permeable and to provide synaptically localized Ca2+ signals that mediate short-term and long-term changes in synaptic strength. Less well known is a subpopulation of AMPA receptors that is Ca2+-permeable and has been shown to be synaptically localized on dorsal horn neurons in culture (Gu et al., 1996) and expressed by dorsal horn neurons in situ (Nagy et al., 1994; Engelman et al., 1997). We used kainate-induced cobalt uptake as a functional marker of neurons expressing Ca2+-permeable AMPA receptors and combined this with markers of nociceptive primary afferents in the postnatal rat dorsal horn. We have shown that cobalt-positive neurons are located in lamina I and outer lamina II, a region strongly innervated by nociceptors. These cobalt-positive neurons colocalize with afferents labeled by LD2, and with the most dorsal region of capsaicin-sensitive and IB4- and LA4-positive afferents. In contrast, inner lamina II has a sparser distribution of cobalt-positive neurons. Some lamina I neurons expressing the NK1 receptor, the receptor for substance P, are also cobalt positive. These neurons are likely to be projection neurons in the nociceptive pathway. On the basis of all of these observations, we propose that Ca2+-permeable AMPA receptors are localized to mediate transmission of nociceptive information.  (+info)

Lateral hypothalamic NMDA receptor subunits NR2A and/or NR2B mediate eating: immunochemical/behavioral evidence. (5/1468)

Cells within the lateral hypothalamic area (LHA) are important in eating control. Glutamate or its analogs, kainic acid (KA) and N-methyl-D-aspartate (NMDA), elicit intense eating when microinjected there, and, conversely, LHA-administered NMDA receptor antagonists suppress deprivation- and NMDA-elicited eating. The subunit composition of LHA NMDA receptors (NMDA-Rs) mediating feeding, however, has not yet been determined. Identifying this is important, because distinct second messengers/modulators may be activated by NMDA-Rs with differing compositions. To begin to address this, we detected LHA NR2A and NR2B subunits by immunoblotting and NR2B subunits by immunohistochemistry using subunit-specific antibodies. To help determine whether NMDA-Rs mediating feeding might contain these subunits, we conducted behavioral studies using LHA-administered ifenprodil, an antagonist selective for NR2A- and/or NR2B-containing NMDA-Rs at the doses we used (0.001-100 nmol). Ifenprodil maximally suppressed NMDA- and deprivation-elicited feeding by 63 and 39%, respectively, but failed to suppress KA-elicited eating, suggesting its actions were behaviorally specific. Collectively, these results suggest that LHA NMDA-Rs, some of which contribute to feeding control, are composed of NR2A and/or NR2B subunits, and implicate NR2A- and/or NR2B-linked signal transduction in feeding behavior.  (+info)

Subtype-specific effects of lithium on glutamate receptor function. (6/1468)

We report that substitution of sodium with lithium (Li+) in the extracellular solution causes subtype-specific changes in the inward and outward currents of glutamate receptors (GluRs), without a shift in reversal potential. Li+ produces an increase of inward and outward currents of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors and decreases in the currents of kainate (KA) and N-methyl-D-aspartate receptors. The greatest effect of Li+ was observed with GluR3. A concentration-response curve for GluR3 reveals that the potentiation caused by Li+ is greatest at saturating agonist concentrations. GluR1, which shows no potentiation by Li+ at 100 microM KA, shows a small but significant potentiation at saturating KA and glutamate concentrations. The effects of Li+ on outward current, where Li+ is not the primary charge carrier, and the lack of reversal potential shift argue for a mechanism of potentiation not associated with Li+ permeation. This potentiation of current is specific for Li+ because rubidium, although causing an increase of inward current, shifted the reversal potential and did not increase outward current. The effects of Li+ are different for KA, a weak desensitizing agonist, and glutamate, a strong desensitizing agonist, suggesting that Li+ might interact with a mechanism of desensitization. By using cyclothiazide (CTZ) to reduce desensitization of GluR3, we find that for low concentrations of KA and glutamate potentiation of the response by a combination of CTZ and Li+ is no greater than by CTZ or Li+ alone. However, at high concentrations of agonist, the potentiation of the response by a combination of CTZ and Li+ is significantly greater than by CTZ or Li+ alone. This potentiation was additive for glutamate but not for KA. At high agonist concentration in the presence of CTZ, the intrinsically lower desensitization produced with KA-evoked responses may preclude Li+ from potentiating the current to the same degree as it can potentiate glutamate-evoked responses. The additive effects of CTZ and Li+ were unique to the flop variant of GluR3.  (+info)

Recurrent mossy fiber pathway in rat dentate gyrus: synaptic currents evoked in presence and absence of seizure-induced growth. (7/1468)

A common feature of temporal lobe epilepsy and of animal models of epilepsy is the growth of hippocampal mossy fibers into the dentate molecular layer, where at least some of them innervate granule cells. Because the mossy fibers are axons of granule cells, the recurrent mossy fiber pathway provides monosynaptic excitatory feedback to these neurons that could facilitate seizure discharge. We used the pilocarpine model of temporal lobe epilepsy to study the synaptic responses evoked by activating this pathway. Whole cell patch-clamp recording demonstrated that antidromic stimulation of the mossy fibers evoked an excitatory postsynaptic current (EPSC) in approximately 74% of granule cells from rats that had survived >10 wk after pilocarpine-induced status epilepticus. Recurrent mossy fiber growth was demonstrated with the Timm stain in all instances. In contrast, antidromic stimulation of the mossy fibers evoked an EPSC in only 5% of granule cells studied 4-6 days after status epilepticus, before recurrent mossy fiber growth became detectable. Notably, antidromic mossy fiber stimulation also evoked an EPSC in many granule cells from control rats. Clusters of mossy fiber-like Timm staining normally were present in the inner third of the dentate molecular layer at the level of the hippocampal formation from which slices were prepared, and several considerations suggested that the recorded EPSCs depended mainly on activation of recurrent mossy fibers rather than associational fibers. In both status epilepticus and control groups, the antidromically evoked EPSC was glutamatergic and involved the activation of both AMPA/kainate and N-methyl-D-aspartate (NMDA) receptors. EPSCs recorded in granule cells from rats with recurrent mossy fiber growth differed in three respects from those recorded in control granule cells: they were much more frequently evoked, a number of them were unusually large, and the NMDA component of the response was generally much more prominent. In contrast to the antidromically evoked EPSC, the EPSC evoked by stimulation of the perforant path appeared to be unaffected by a prior episode of status epilepticus. These results support the hypothesis that recurrent mossy fiber growth and synapse formation increases the excitatory drive to dentate granule cells and thus facilitates repetitive synchronous discharge. Activation of NMDA receptors in the recurrent pathway may contribute to seizure propagation under depolarizing conditions. Mossy fiber-granule cell synapses also are present in normal rats, where they may contribute to repetitive granule cell discharge in regions of the dentate gyrus where their numbers are significant.  (+info)

Role of the Botzinger complex in fastigial nucleus-mediated respiratory responses. (8/1468)

We have reported that the phrenic neurogram (PN) is modulated by stimulation of the fastigial nucleus (FN) of the cerebellum. The present study was undertaken to search for brainstem site(s) involved in the FN efferent pathway to modulate phrenic nerve activities. Experiments were performed on 35 anesthetized, paralyzed, and ventilated cats, using the PN as the index of the respiratory motor output. Results showed that bilateral electrolytic lesions of the red nucleus (RN), the paramedian reticular nucleus (PRN), or the pontine respiratory group (PRG) had little effect on the ability of FN stimulation to modulate the respiratory output. However, the modulation was abolished by bilateral electrolytic lesions of the Botzinger complex (BotC). Further studies showed that bilateral chemical inactivation of BotC neurons produced by topical microinjection of kainic acid or cobalt chloride failed to abolish the modulation. We concluded that fibers of passage, not synapses or cell bodies in the BotC, were involved in the modulatory effect of FN stimulation on the PN. The RN, PRN, and PRG appear not to be important in the neural circuitry responsible for the FN modulation of the phrenic activity.  (+info)

Kainic acid is not a medical term per se, but it is a compound that has been widely used in scientific research, particularly in neuroscience. It is a type of excitatory amino acid that acts as an agonist at certain types of receptors in the brain, specifically the AMPA and kainate receptors.

Kainic acid is often used in research to study the effects of excitotoxicity, which is a process that occurs when nerve cells are exposed to excessive amounts of glutamate or other excitatory neurotransmitters, leading to cell damage or death. Kainic acid can induce seizures and other neurological symptoms in animals, making it a valuable tool for studying epilepsy and related disorders.

While kainic acid itself is not a medical treatment or diagnosis, understanding its effects on the brain has contributed to our knowledge of neurological diseases and potential targets for therapy.

Excitatory amino acid agonists are substances that bind to and activate excitatory amino acid receptors, leading to an increase in the excitation or activation of neurons. The most common excitatory amino acids in the central nervous system are glutamate and aspartate.

Agonists of excitatory amino acid receptors can be divided into two main categories: ionotropic and metabotropic. Ionotropic receptors, such as N-methyl-D-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainite receptors, are ligand-gated ion channels that directly mediate fast excitatory synaptic transmission. Metabotropic receptors, on the other hand, are G protein-coupled receptors that modulate synaptic activity through second messenger systems.

Excitatory amino acid agonists have been implicated in various physiological and pathophysiological processes, including learning and memory, neurodevelopment, and neurodegenerative disorders such as stroke, epilepsy, and Alzheimer's disease. They are also used in research to study the functions of excitatory amino acid receptors and their roles in neuronal signaling. However, due to their potential neurotoxic effects, the therapeutic use of excitatory amino acid agonists is limited.

A seizure is an uncontrolled, abnormal firing of neurons (brain cells) that can cause various symptoms such as convulsions, loss of consciousness, altered awareness, or changes in behavior. Seizures can be caused by a variety of factors including epilepsy, brain injury, infection, toxic substances, or genetic disorders. They can also occur without any identifiable cause, known as idiopathic seizures. Seizures are a medical emergency and require immediate attention.

Kainic acid receptors are a type of ionotropic glutamate receptor that are widely distributed in the central nervous system. They are named after kainic acid, a neuroexcitatory compound that binds to and activates these receptors. Kainic acid receptors play important roles in excitatory synaptic transmission, neuronal development, and synaptic plasticity.

Kainic acid receptors are composed of five subunits, which can be assembled from various combinations of GluK1-5 (also known as GluR5-7 and KA1-2) subunits. These subunits have different properties and contribute to the functional diversity of kainic acid receptors.

Activation of kainic acid receptors leads to an influx of calcium ions, which can trigger various intracellular signaling pathways and modulate synaptic strength. Dysregulation of kainic acid receptor function has been implicated in several neurological disorders, including epilepsy, pain, ischemia, and neurodegenerative diseases.

Status epilepticus is a serious and life-threatening medical condition characterized by an ongoing seizure activity or a series of seizures without full recovery of consciousness between them, lasting for 30 minutes or more. It is a neurological emergency that requires immediate medical attention to prevent potential complications such as brain damage, respiratory failure, or even death.

The condition can occur in people with a history of epilepsy or seizure disorders, as well as those without any prior history of seizures. The underlying causes of status epilepticus can vary and may include infection, trauma, stroke, metabolic imbalances, toxins, or other medical conditions that affect the brain's normal functioning. Prompt diagnosis and treatment are crucial to prevent long-term neurological damage and improve outcomes in patients with this condition.

The hippocampus is a complex, curved formation in the brain that resembles a seahorse (hence its name, from the Greek word "hippos" meaning horse and "kampos" meaning sea monster). It's part of the limbic system and plays crucial roles in the formation of memories, particularly long-term ones.

This region is involved in spatial navigation and cognitive maps, allowing us to recognize locations and remember how to get to them. Additionally, it's one of the first areas affected by Alzheimer's disease, which often results in memory loss as an early symptom.

Anatomically, it consists of two main parts: the Ammon's horn (or cornu ammonis) and the dentate gyrus. These structures are made up of distinct types of neurons that contribute to different aspects of learning and memory.

Convulsants are substances or agents that can cause seizures or convulsions. These can be medications, toxins, or illnesses that lower the seizure threshold and lead to abnormal electrical activity in the brain, resulting in uncontrolled muscle contractions and relaxation. Examples of convulsants include bromides, strychnine, organophosphate pesticides, certain antibiotics (such as penicillin or cephalosporins), and alcohol withdrawal. It is important to note that some medications used to treat seizures can also have convulsant properties at higher doses or in overdose situations.

Flurothyl, also known as Nelson's fluid or induction agent, is a chemical compound with the formula C5H4F6O. It is a colorless liquid that is volatile and has a sweetish odor. In medicine, it was historically used as a rapid-acting inhalational general anesthetic, but its use has been largely discontinued due to safety concerns, including the risk of seizures and cardiac arrest. Flurothyl works by sensitizing the brain to carbon dioxide, leading to a loss of consciousness. It is still used in research settings to study seizure disorders and anesthetic mechanisms.

N-Methyl-D-Aspartate (NMDA) is not a medication but a type of receptor, specifically a glutamate receptor, found in the post-synaptic membrane in the central nervous system. Glutamate is a major excitatory neurotransmitter in the brain. NMDA receptors are involved in various functions such as synaptic plasticity, learning, and memory. They also play a role in certain neurological disorders like epilepsy, neurodegenerative diseases, and chronic pain.

NMDA receptors are named after N-Methyl-D-Aspartate, a synthetic analog of the amino acid aspartic acid, which is a selective agonist for this type of receptor. An agonist is a substance that binds to a receptor and causes a response similar to that of the natural ligand (in this case, glutamate).

Neurons, also known as nerve cells or neurocytes, are specialized cells that constitute the basic unit of the nervous system. They are responsible for receiving, processing, and transmitting information and signals within the body. Neurons have three main parts: the dendrites, the cell body (soma), and the axon. The dendrites receive signals from other neurons or sensory receptors, while the axon transmits these signals to other neurons, muscles, or glands. The junction between two neurons is called a synapse, where neurotransmitters are released to transmit the signal across the gap (synaptic cleft) to the next neuron. Neurons vary in size, shape, and structure depending on their function and location within the nervous system.

Neurotoxins are substances that are poisonous or destructive to nerve cells (neurons) and the nervous system. They can cause damage by destroying neurons, disrupting communication between neurons, or interfering with the normal functioning of the nervous system. Neurotoxins can be produced naturally by certain organisms, such as bacteria, plants, and animals, or they can be synthetic compounds created in a laboratory. Examples of neurotoxins include botulinum toxin (found in botulism), tetrodotoxin (found in pufferfish), and heavy metals like lead and mercury. Neurotoxic effects can range from mild symptoms such as headaches, muscle weakness, and tremors, to more severe symptoms such as paralysis, seizures, and cognitive impairment. Long-term exposure to neurotoxins can lead to chronic neurological conditions and other health problems.

Kindling, in the context of neurology, refers to a process of neural sensitization where repeated exposure to sub-convulsive stimuli below the threshold for triggering a seizure can eventually lower this threshold, leading to an increased susceptibility to develop seizures. This concept is often applied in the study of epilepsy and other neuropsychiatric disorders.

The term "kindling" was first introduced by Racine in 1972 to describe the progressive increase in the severity and duration of behavioral responses following repeated electrical stimulation of the brain in animal models. The kindling process can occur in response to various types of stimuli, including electrical, chemical, or even environmental stimuli, leading to changes in neuronal excitability and synaptic plasticity in certain brain regions, particularly the limbic system.

Over time, repeated stimulation results in a permanent increase in neural hypersensitivity, making it easier to induce seizures with weaker stimuli. This phenomenon has been implicated in the development and progression of some forms of epilepsy, as well as in the underlying mechanisms of certain mood disorders and other neurological conditions.

Pentylenetetrazole (PTZ) is not primarily considered a medical treatment, but rather a research compound used in neuroscience and neurology to study seizure activity and chemically induce seizures in animals for experimental purposes. It is classified as a proconvulsant agent. Medically, it has been used in the past as a medication to treat epilepsy, but its use is now largely historical due to the availability of safer and more effective anticonvulsant drugs.

In a medical or scientific context, Pentylenetetrazole can be defined as:

A chemical compound with the formula C6H5N5O2, which is used in research to investigate seizure activity and induce convulsions in animals. It acts as a non-competitive GABAA receptor antagonist and can lower the seizure threshold. Historically, it has been used as a medication to treat epilepsy, but its use for this purpose is now limited due to the development of safer and more effective anticonvulsant drugs.

The medulla oblongata is a part of the brainstem that is located in the posterior portion of the brainstem and continues with the spinal cord. It plays a vital role in controlling several critical bodily functions, such as breathing, heart rate, and blood pressure. The medulla oblongata also contains nerve pathways that transmit sensory information from the body to the brain and motor commands from the brain to the muscles. Additionally, it is responsible for reflexes such as vomiting, swallowing, coughing, and sneezing.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Temporal lobe epilepsy (TLE) is a type of focal (localized) epilepsy that originates from the temporal lobes of the brain. The temporal lobes are located on each side of the brain and are involved in processing sensory information, memory, and emotion. TLE is characterized by recurrent seizures that originate from one or both temporal lobes.

The symptoms of TLE can vary depending on the specific area of the temporal lobe that is affected. However, common symptoms include auras (sensory or emotional experiences that occur before a seizure), strange smells or tastes, lip-smacking or chewing movements, and memory problems. Some people with TLE may also experience automatisms (involuntary movements such as picking at clothes or fumbling with objects) during their seizures.

Treatment for TLE typically involves medication to control seizures, although surgery may be recommended in some cases. The goal of treatment is to reduce the frequency and severity of seizures and improve quality of life.

Neurotransmitter receptors are specialized protein molecules found on the surface of neurons and other cells in the body. They play a crucial role in chemical communication within the nervous system by binding to specific neurotransmitters, which are chemicals that transmit signals across the synapse (the tiny gap between two neurons).

When a neurotransmitter binds to its corresponding receptor, it triggers a series of biochemical events that can either excite or inhibit the activity of the target neuron. This interaction helps regulate various physiological processes, including mood, cognition, movement, and sensation.

Neurotransmitter receptors can be classified into two main categories based on their mechanism of action: ionotropic and metabotropic receptors. Ionotropic receptors are ligand-gated ion channels that directly allow ions to flow through the cell membrane upon neurotransmitter binding, leading to rapid changes in neuronal excitability. In contrast, metabotropic receptors are linked to G proteins and second messenger systems, which modulate various intracellular signaling pathways more slowly.

Examples of neurotransmitters include glutamate, GABA (gamma-aminobutyric acid), dopamine, serotonin, acetylcholine, and norepinephrine, among others. Each neurotransmitter has its specific receptor types, which may have distinct functions and distributions within the nervous system. Understanding the roles of these receptors and their interactions with neurotransmitters is essential for developing therapeutic strategies to treat various neurological and psychiatric disorders.

Quinolinic acid is a type of organic compound that belongs to the class of heterocyclic compounds known as quinolines, which contain a bicyclic system made up of a benzene ring fused to a piperidine ring. Quinolinic acid is specifically a derivative of quinoline with a carboxylic acid functional group.

In the context of medicine and biology, quinolinic acid is an endogenous excitatory neurotransmitter and a metabolite in the kynurenine pathway of tryptophan metabolism. It is mainly produced in the brain by activated microglia and to some extent by macrophages, neurons, and astrocytes.

Quinolinic acid has been implicated in several neurological disorders, including Huntington's disease, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), HIV-associated dementia, and depression. High levels of quinolinic acid can cause excitotoxicity, which is a process of neurotoxicity induced by excessive stimulation of glutamate receptors leading to neuronal damage or death. It has also been suggested that quinolinic acid may play a role in the pathogenesis of some psychiatric disorders, such as schizophrenia and bipolar disorder.

Nitrergic neurons are specialized cells within the nervous system that release nitric oxide (NO) as their primary neurotransmitter. Nitric oxide is a small, gaseous molecule that plays an essential role in various physiological processes, including neurotransmission, vasodilation, and immune response.

In the context of the nervous system, nitrergic neurons are involved in several functions:

1. Neurotransmission: Nitric oxide acts as a retrograde messenger, transmitting signals backward across synapses to modulate the activity of presynaptic neurons. This unique mode of communication allows for fine-tuning of neural circuits and contributes to various cognitive processes, such as learning and memory.
2. Vasodilation: Nitrergic neurons are present in blood vessel walls, where they release nitric oxide to cause vasodilation. This process helps regulate blood flow and pressure in different organs and tissues.
3. Immune response: Nitrergic neurons can interact with immune cells, releasing nitric oxide to modulate their activity and contribute to the body's defense mechanisms.
4. Gastrointestinal motility: In the gastrointestinal tract, nitrergic neurons are involved in regulating smooth muscle contractility and relaxation, which influences gut motility and secretion.
5. Reproductive system function: Nitrergic neurons play a role in the regulation of sexual behavior, penile erection, and sperm motility in the male reproductive system.

It is important to note that nitrergic neurons can be found throughout the nervous system, including the central and peripheral nervous systems, and are involved in various physiological processes. Dysfunction of these neurons has been implicated in several pathological conditions, such as neurodegenerative diseases, cardiovascular disorders, and gastrointestinal motility dysfunctions.

Ibotenic acid is a naturally occurring neurotoxin that can be found in certain species of mushrooms, including the Amanita muscaria and Amanita pantherina. It is a type of glutamate receptor agonist, which means it binds to and activates certain receptors in the brain called N-methyl-D-aspartate (NMDA) receptors.

Ibotenic acid has been used in scientific research as a tool for studying the brain and nervous system. It can cause excitotoxicity, which is a process of excessive stimulation of nerve cells leading to their damage or death. This property has been exploited in studies involving neurodegenerative disorders, where ibotenic acid is used to selectively destroy specific populations of neurons to understand the functional consequences and potential therapeutic interventions for these conditions.

However, it's important to note that ibotenic acid is not used as a treatment or therapy in humans due to its neurotoxic effects. It should only be handled and used by trained professionals in controlled laboratory settings for research purposes.

Epilepsy is a chronic neurological disorder characterized by recurrent, unprovoked seizures. These seizures are caused by abnormal electrical activity in the brain, which can result in a wide range of symptoms, including convulsions, loss of consciousness, and altered sensations or behaviors. Epilepsy can have many different causes, including genetic factors, brain injury, infection, or stroke. In some cases, the cause may be unknown.

There are many different types of seizures that can occur in people with epilepsy, and the specific type of seizure will depend on the location and extent of the abnormal electrical activity in the brain. Some people may experience only one type of seizure, while others may have several different types. Seizures can vary in frequency, from a few per year to dozens or even hundreds per day.

Epilepsy is typically diagnosed based on the patient's history of recurrent seizures and the results of an electroencephalogram (EEG), which measures the electrical activity in the brain. Imaging tests such as MRI or CT scans may also be used to help identify any structural abnormalities in the brain that may be contributing to the seizures.

While there is no cure for epilepsy, it can often be effectively managed with medication. In some cases, surgery may be recommended to remove the area of the brain responsible for the seizures. With proper treatment and management, many people with epilepsy are able to lead normal, productive lives.

Alpha-Methyltyrosine (α-MT) is a synthetic amino acid that acts as an inhibitor of the enzyme tyrosine hydroxylase. This enzyme is a rate-limiting step in the biosynthesis of catecholamines, including neurotransmitters such as dopamine and norepinephrine. By inhibiting tyrosine hydroxylase, α-MT reduces the synthesis of these catecholamines, which can lead to various effects on the nervous system.

In medical contexts, α-MT has been used in research settings to study the functions of catecholamines and their role in various physiological processes. It has also been investigated as a potential treatment for certain conditions, such as hypertension and anxiety disorders, although its clinical use is not widespread due to its side effects and limited efficacy.

It's important to note that α-MT should only be used under the supervision of a medical professional, as it can have significant effects on the nervous system and may interact with other medications or health conditions.

Mossy fibers in the hippocampus are a type of axon that originates from granule cells located in the dentate gyrus, which is the first part of the hippocampus. These fibers have a distinctive appearance and earn their name from the numerous small branches or "spines" that cover their surface, giving them a bushy or "mossy" appearance.

Mossy fibers form excitatory synapses with pyramidal cells in the CA3 region of the hippocampus, which is involved in memory and spatial navigation. These synapses are unique because they have a high degree of plasticity, meaning that they can change their strength in response to experience or learning. This plasticity is thought to be important for the formation and storage of memories.

Mossy fibers also release neurotransmitters such as glutamate and contribute to the regulation of hippocampal excitability. Dysfunction in mossy fiber function has been implicated in several neurological disorders, including epilepsy and Alzheimer's disease.

Glutamate receptors are a type of neuroreceptor in the central nervous system that bind to the neurotransmitter glutamate. They play a crucial role in excitatory synaptic transmission, plasticity, and neuronal development. There are several types of glutamate receptors, including ionotropic and metabotropic receptors, which can be further divided into subclasses based on their pharmacological properties and molecular structure.

Ionotropic glutamate receptors, also known as iGluRs, are ligand-gated ion channels that directly mediate fast synaptic transmission. They include N-methyl-D-aspartate (NMDA) receptors, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, and kainite receptors.

Metabotropic glutamate receptors, also known as mGluRs, are G protein-coupled receptors that modulate synaptic transmission through second messenger systems. They include eight subtypes (mGluR1-8) that are classified into three groups based on their sequence homology, pharmacological properties, and signal transduction mechanisms.

Glutamate receptors have been implicated in various physiological processes, including learning and memory, motor control, sensory perception, and emotional regulation. Dysfunction of glutamate receptors has also been associated with several neurological disorders, such as epilepsy, Alzheimer's disease, Parkinson's disease, and psychiatric conditions like schizophrenia and depression.

The vestibular nuclei are clusters of neurons located in the brainstem that receive and process information from the vestibular system, which is responsible for maintaining balance and spatial orientation. The vestibular nuclei help to coordinate movements of the eyes, head, and body in response to changes in position or movement. They also play a role in reflexes that help to maintain posture and stabilize vision during head movement. There are four main vestibular nuclei: the medial, lateral, superior, and inferior vestibular nuclei.

Glutamates are the salt or ester forms of glutamic acid, which is a naturally occurring amino acid and the most abundant excitatory neurotransmitter in the central nervous system. Glutamate plays a crucial role in various brain functions, such as learning, memory, and cognition. However, excessive levels of glutamate can lead to neuronal damage or death, contributing to several neurological disorders, including stroke, epilepsy, and neurodegenerative diseases like Alzheimer's and Parkinson's.

Glutamates are also commonly found in food as a natural flavor enhancer, often listed under the name monosodium glutamate (MSG). While MSG has been extensively studied, its safety remains a topic of debate, with some individuals reporting adverse reactions after consuming foods containing this additive.

Pyrrolidines are not a medical term per se, but they are a chemical compound that can be encountered in the field of medicine and pharmacology. Pyrrolidine is an organic compound with the molecular formula (CH2)4NH. It is a cyclic secondary amine, which means it contains a nitrogen atom surrounded by four carbon atoms in a ring structure.

Pyrrolidines can be found in certain natural substances and are also synthesized for use in pharmaceuticals and research. They have been used as building blocks in the synthesis of various drugs, including some muscle relaxants, antipsychotics, and antihistamines. Additionally, pyrrolidine derivatives can be found in certain plants and fungi, where they may contribute to biological activity or toxicity.

It is important to note that while pyrrolidines themselves are not a medical condition or diagnosis, understanding their chemical properties and uses can be relevant to the study and development of medications.

Nerve degeneration, also known as neurodegeneration, is the progressive loss of structure and function of neurons, which can lead to cognitive decline, motor impairment, and various other symptoms. This process occurs due to a variety of factors, including genetics, environmental influences, and aging. It is a key feature in several neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and multiple sclerosis. The degeneration can affect any part of the nervous system, leading to different symptoms depending on the location and extent of the damage.

Gliosis is a term used in histopathology and neuroscience to describe the reaction of support cells in the brain, called glial cells, to injury or disease. This response includes an increase in the number and size of glial cells, as well as changes in their shape and function. The most common types of glial cells involved in gliosis are astrocytes and microglia.

Gliosis can be triggered by a variety of factors, including trauma, infection, inflammation, neurodegenerative diseases, and stroke. In response to injury or disease, astrocytes become hypertrophied (enlarged) and undergo changes in their gene expression profile that can lead to the production of various proteins, such as glial fibrillary acidic protein (GFAP). These changes can result in the formation of a dense network of astrocytic processes, which can contribute to the formation of a glial scar.

Microglia, another type of glial cell, become activated during gliosis and play a role in the immune response in the central nervous system (CNS). They can release pro-inflammatory cytokines, chemokines, and reactive oxygen species that contribute to the inflammatory response.

While gliosis is a protective response aimed at containing damage and promoting tissue repair, it can also have negative consequences. For example, the formation of glial scars can impede axonal regeneration and contribute to neurological deficits. Additionally, chronic activation of microglia has been implicated in various neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease.

Glutamic acid is an alpha-amino acid, which is one of the 20 standard amino acids in the genetic code. The systematic name for this amino acid is (2S)-2-Aminopentanedioic acid. Its chemical formula is HO2CCH(NH2)CH2CH2CO2H.

Glutamic acid is a crucial excitatory neurotransmitter in the human brain, and it plays an essential role in learning and memory. It's also involved in the metabolism of sugars and amino acids, the synthesis of proteins, and the removal of waste nitrogen from the body.

Glutamic acid can be found in various foods such as meat, fish, beans, eggs, dairy products, and vegetables. In the human body, glutamic acid can be converted into gamma-aminobutyric acid (GABA), another important neurotransmitter that has a calming effect on the nervous system.

I'm sorry for any confusion, but Quisqualic Acid is not a commonly used term in medicine or medical research. It is actually a type of neurotoxin that comes from certain plants and has been used in scientific research related to the nervous system and brain function. However, it is not something that would typically be discussed in a medical context for patient care or treatment.

Neuroprotective agents are substances that protect neurons or nerve cells from damage, degeneration, or death caused by various factors such as trauma, inflammation, oxidative stress, or excitotoxicity. These agents work through different mechanisms, including reducing the production of free radicals, inhibiting the release of glutamate (a neurotransmitter that can cause cell damage in high concentrations), promoting the growth and survival of neurons, and preventing apoptosis (programmed cell death). Neuroprotective agents have been studied for their potential to treat various neurological disorders, including stroke, traumatic brain injury, Parkinson's disease, Alzheimer's disease, and multiple sclerosis. However, more research is needed to fully understand their mechanisms of action and to develop effective therapies.

The periaqueductal gray (PAG) is a region in the midbrain, surrounding the cerebral aqueduct (a narrow channel connecting the third and fourth ventricles within the brain). It is a column of neurons that plays a crucial role in the modulation of pain perception, cardiorespiratory regulation, and defensive behaviors. The PAG is involved in the descending pain modulatory system, where it receives input from various emotional and cognitive areas and sends output to the rostral ventromedial medulla, which in turn regulates nociceptive processing at the spinal cord level. Additionally, the PAG is implicated in the regulation of fear, anxiety, and stress responses, as well as sexual behavior and reward processing.

The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:

1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.

The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) is a type of excitatory amino acid that functions as a neurotransmitter in the central nervous system. It plays a crucial role in fast synaptic transmission and plasticity in the brain. AMPA receptors are ligand-gated ion channels that are activated by the binding of glutamate or AMPA, allowing the flow of sodium and potassium ions across the neuronal membrane. This ion flux leads to the depolarization of the postsynaptic neuron and the initiation of action potentials. AMPA receptors are also targets for various drugs and toxins that modulate synaptic transmission and plasticity in the brain.

Quinolinic acid is a metabolite found in the human body, produced during the metabolism of tryptophan, an essential amino acid. It is a component of the kynurenine pathway and acts as a neuroexcitatory chemical in the brain. In excessive amounts, quinolinic acid can lead to neurotoxicity, causing damage to neurons and contributing to several neurological disorders such as Huntington's disease, Alzheimer's disease, Parkinson's disease, AIDS-dementia complex, and multiple sclerosis. It also plays a role in the pathogenesis of psychiatric conditions like schizophrenia and major depressive disorder.

"Inbred strains of rats" are genetically identical rodents that have been produced through many generations of brother-sister mating. This results in a high degree of homozygosity, where the genes at any particular locus in the genome are identical in all members of the strain.

Inbred strains of rats are widely used in biomedical research because they provide a consistent and reproducible genetic background for studying various biological phenomena, including the effects of drugs, environmental factors, and genetic mutations on health and disease. Additionally, inbred strains can be used to create genetically modified models of human diseases by introducing specific mutations into their genomes.

Some commonly used inbred strains of rats include the Wistar Kyoto (WKY), Sprague-Dawley (SD), and Fischer 344 (F344) rat strains. Each strain has its own unique genetic characteristics, making them suitable for different types of research.

Anticonvulsants are a class of drugs used primarily to treat seizure disorders, also known as epilepsy. These medications work by reducing the abnormal electrical activity in the brain that leads to seizures. In addition to their use in treating epilepsy, anticonvulsants are sometimes also prescribed for other conditions, such as neuropathic pain, bipolar disorder, and migraine headaches.

Anticonvulsants can work in different ways to reduce seizure activity. Some medications, such as phenytoin and carbamazepine, work by blocking sodium channels in the brain, which helps to stabilize nerve cell membranes and prevent excessive electrical activity. Other medications, such as valproic acid and gabapentin, increase the levels of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain, which has a calming effect on nerve cells and helps to reduce seizure activity.

While anticonvulsants are generally effective at reducing seizure frequency and severity, they can also have side effects, such as dizziness, drowsiness, and gastrointestinal symptoms. In some cases, these side effects may be managed by adjusting the dosage or switching to a different medication. It is important for individuals taking anticonvulsants to work closely with their healthcare provider to monitor their response to the medication and make any necessary adjustments.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Excitatory amino acids (EAAs) are a type of neurotransmitter, which are chemical messengers that transmit signals in the brain and nervous system. The most important excitatory amino acids in the central nervous system are glutamate and aspartate. These neurotransmitters play crucial roles in various physiological functions such as learning, memory, and synaptic plasticity. However, excessive or prolonged activation of EAA receptors can lead to neuronal damage or death, which is thought to contribute to several neurological disorders, including stroke, epilepsy, and neurodegenerative diseases.

Cell death is the process by which cells cease to function and eventually die. There are several ways that cells can die, but the two most well-known and well-studied forms of cell death are apoptosis and necrosis.

Apoptosis is a programmed form of cell death that occurs as a normal and necessary process in the development and maintenance of healthy tissues. During apoptosis, the cell's DNA is broken down into small fragments, the cell shrinks, and the membrane around the cell becomes fragmented, allowing the cell to be easily removed by phagocytic cells without causing an inflammatory response.

Necrosis, on the other hand, is a form of cell death that occurs as a result of acute tissue injury or overwhelming stress. During necrosis, the cell's membrane becomes damaged and the contents of the cell are released into the surrounding tissue, causing an inflammatory response.

There are also other forms of cell death, such as autophagy, which is a process by which cells break down their own organelles and proteins to recycle nutrients and maintain energy homeostasis, and pyroptosis, which is a form of programmed cell death that occurs in response to infection and involves the activation of inflammatory caspases.

Cell death is an important process in many physiological and pathological processes, including development, tissue homeostasis, and disease. Dysregulation of cell death can contribute to the development of various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases.

Physiologic nystagmus is a type of normal, involuntary eye movement that occurs in certain situations. It is characterized by rhythmical to-and-fro movements of the eyes, which can be horizontal, vertical, or rotatory. The most common form of physiologic nystagmus is called "optokinetic nystagmus," which occurs when a person looks at a moving pattern, such as stripes on a rotating drum or scenery passing by a car window.

Optokinetic nystagmus helps to stabilize the image of the environment on the retina and allows the brain to perceive motion accurately. Another form of physiologic nystagmus is "pursuit nystagmus," which occurs when the eyes attempt to follow a slowly moving target. In this case, the eyes may overshoot the target and then make a corrective movement in the opposite direction.

Physiologic nystagmus is different from pathological nystagmus, which can be caused by various medical conditions such as brain damage, inner ear disorders, or medications that affect the nervous system. Pathological nystagmus may indicate a serious underlying condition and should be evaluated by a healthcare professional.

N-Methyl-D-Aspartate (NMDA) receptors are a type of ionotropic glutamate receptor, which are found in the membranes of excitatory neurons in the central nervous system. They play a crucial role in synaptic plasticity, learning, and memory processes. NMDA receptors are ligand-gated channels that are permeable to calcium ions (Ca2+) and other cations.

NMDA receptors are composed of four subunits, which can be a combination of NR1, NR2A-D, and NR3A-B subunits. The binding of the neurotransmitter glutamate to the NR2 subunit and glycine to the NR1 subunit leads to the opening of the ion channel and the influx of Ca2+ ions.

NMDA receptors have a unique property in that they require both agonist binding and membrane depolarization for full activation, making them sensitive to changes in the electrical activity of the neuron. This property allows NMDA receptors to act as coincidence detectors, playing a critical role in synaptic plasticity and learning.

Abnormal functioning of NMDA receptors has been implicated in various neurological disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, and chronic pain. Therefore, NMDA receptors are a common target for drug development in the treatment of these conditions.

Hyperprolactinemia is a medical condition characterized by abnormally high levels of prolactin, a hormone produced by the pituitary gland. In women, this can lead to menstrual irregularities, milk production outside of pregnancy (galactorrhea), and infertility. In men, it can cause decreased libido, erectile dysfunction, breast enlargement (gynecomastia), and infertility. The condition can be caused by various factors, including pituitary tumors, certain medications, and hypothyroidism. Treatment typically involves addressing the underlying cause and may include medication to lower prolactin levels.

Microinjection is a medical technique that involves the use of a fine, precise needle to inject small amounts of liquid or chemicals into microscopic structures, cells, or tissues. This procedure is often used in research settings to introduce specific substances into individual cells for study purposes, such as introducing DNA or RNA into cell nuclei to manipulate gene expression.

In clinical settings, microinjections may be used in various medical and cosmetic procedures, including:

1. Intracytoplasmic Sperm Injection (ICSI): A type of assisted reproductive technology where a single sperm is injected directly into an egg to increase the chances of fertilization during in vitro fertilization (IVF) treatments.
2. Botulinum Toxin Injections: Microinjections of botulinum toxin (Botox, Dysport, or Xeomin) are used for cosmetic purposes to reduce wrinkles and fine lines by temporarily paralyzing the muscles responsible for their formation. They can also be used medically to treat various neuromuscular disorders, such as migraines, muscle spasticity, and excessive sweating (hyperhidrosis).
3. Drug Delivery: Microinjections may be used to deliver drugs directly into specific tissues or organs, bypassing the systemic circulation and potentially reducing side effects. This technique can be particularly useful in treating localized pain, delivering growth factors for tissue regeneration, or administering chemotherapy agents directly into tumors.
4. Gene Therapy: Microinjections of genetic material (DNA or RNA) can be used to introduce therapeutic genes into cells to treat various genetic disorders or diseases, such as cystic fibrosis, hemophilia, or cancer.

Overall, microinjection is a highly specialized and precise technique that allows for the targeted delivery of substances into small structures, cells, or tissues, with potential applications in research, medical diagnostics, and therapeutic interventions.

Intraventricular injections are a type of medical procedure where medication is administered directly into the cerebral ventricles of the brain. The cerebral ventricles are fluid-filled spaces within the brain that contain cerebrospinal fluid (CSF). This procedure is typically used to deliver drugs that target conditions affecting the central nervous system, such as infections or tumors.

Intraventricular injections are usually performed using a thin, hollow needle that is inserted through a small hole drilled into the skull. The medication is then injected directly into the ventricles, allowing it to circulate throughout the CSF and reach the brain tissue more efficiently than other routes of administration.

This type of injection is typically reserved for situations where other methods of drug delivery are not effective or feasible. It carries a higher risk of complications, such as bleeding, infection, or damage to surrounding tissues, compared to other routes of administration. Therefore, it is usually performed by trained medical professionals in a controlled clinical setting.

Electroencephalography (EEG) is a medical procedure that records electrical activity in the brain. It uses small, metal discs called electrodes, which are attached to the scalp with paste or a specialized cap. These electrodes detect tiny electrical charges that result from the activity of brain cells, and the EEG machine then amplifies and records these signals.

EEG is used to diagnose various conditions related to the brain, such as seizures, sleep disorders, head injuries, infections, and degenerative diseases like Alzheimer's or Parkinson's. It can also be used during surgery to monitor brain activity and ensure that surgical procedures do not interfere with vital functions.

EEG is a safe and non-invasive procedure that typically takes about 30 minutes to an hour to complete, although longer recordings may be necessary in some cases. Patients are usually asked to relax and remain still during the test, as movement can affect the quality of the recording.

The dentate gyrus is a region of the brain that is located in the hippocampal formation, which is a part of the limbic system and plays a crucial role in learning, memory, and spatial navigation. It is characterized by the presence of densely packed granule cells, which are a type of neuron. The dentate gyrus is involved in the formation of new memories and the integration of information from different brain regions. It is also one of the few areas of the adult brain where new neurons can be generated throughout life, a process known as neurogenesis. Damage to the dentate gyrus has been linked to memory impairments, cognitive decline, and neurological disorders such as Alzheimer's disease and epilepsy.

The pons is a part of the brainstem that lies between the medulla oblongata and the midbrain. Its name comes from the Latin word "ponte" which means "bridge," as it serves to connect these two regions of the brainstem. The pons contains several important structures, including nerve fibers that carry signals between the cerebellum (the part of the brain responsible for coordinating muscle movements) and the rest of the nervous system. It also contains nuclei (clusters of neurons) that help regulate various functions such as respiration, sleep, and facial movements.

Pilocarpine is a cholinergic agonist, which means it stimulates the parasympathetic nervous system by binding to muscarinic receptors. It is primarily used in the treatment of dry mouth (xerostomia) caused by radiation therapy or Sjögren's syndrome, as well as in the management of glaucoma due to its ability to construct the pupils and reduce intraocular pressure. Pilocarpine can also be used to treat certain cardiovascular conditions and chronic bronchitis. It is available in various forms, including tablets, ophthalmic solutions, and topical gels.

Excitatory amino acid antagonists are a class of drugs that block the action of excitatory neurotransmitters, particularly glutamate and aspartate, in the brain. These drugs work by binding to and blocking the receptors for these neurotransmitters, thereby reducing their ability to stimulate neurons and produce an excitatory response.

Excitatory amino acid antagonists have been studied for their potential therapeutic benefits in a variety of neurological conditions, including stroke, epilepsy, traumatic brain injury, and neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. However, their use is limited by the fact that blocking excitatory neurotransmission can also have negative effects on cognitive function and memory.

There are several types of excitatory amino acid receptors, including N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainite receptors. Different excitatory amino acid antagonists may target one or more of these receptor subtypes, depending on their specific mechanism of action.

Examples of excitatory amino acid antagonists include ketamine, memantine, and dextromethorphan. These drugs have been used in clinical practice for various indications, such as anesthesia, sedation, and treatment of neurological disorders. However, their use must be carefully monitored due to potential side effects and risks associated with blocking excitatory neurotransmission.

The corpus striatum is a part of the brain that plays a crucial role in movement, learning, and cognition. It consists of two structures called the caudate nucleus and the putamen, which are surrounded by the external and internal segments of the globus pallidus. Together, these structures form the basal ganglia, a group of interconnected neurons that help regulate voluntary movement.

The corpus striatum receives input from various parts of the brain, including the cerebral cortex, thalamus, and other brainstem nuclei. It processes this information and sends output to the globus pallidus and substantia nigra, which then project to the thalamus and back to the cerebral cortex. This feedback loop helps coordinate and fine-tune movements, allowing for smooth and coordinated actions.

Damage to the corpus striatum can result in movement disorders such as Parkinson's disease, Huntington's disease, and dystonia. These conditions are characterized by abnormal involuntary movements, muscle stiffness, and difficulty initiating or controlling voluntary movements.

'Animal behavior' refers to the actions or responses of animals to various stimuli, including their interactions with the environment and other individuals. It is the study of the actions of animals, whether they are instinctual, learned, or a combination of both. Animal behavior includes communication, mating, foraging, predator avoidance, and social organization, among other things. The scientific study of animal behavior is called ethology. This field seeks to understand the evolutionary basis for behaviors as well as their physiological and psychological mechanisms.

6-Cyano-7-nitroquinoxaline-2,3-dione is a chemical compound that is commonly used in research and scientific studies. It is a member of the quinoxaline family of compounds, which are aromatic heterocyclic organic compounds containing two nitrogen atoms.

The 6-Cyano-7-nitroquinoxaline-2,3-dione compound has several notable features, including:

* A quinoxaline ring structure, which is made up of two benzene rings fused to a pyrazine ring.
* A cyano group (-CN) at the 6th position of the quinoxaline ring.
* A nitro group (-NO2) at the 7th position of the quinoxaline ring.
* Two carbonyl groups (=O) at the 2nd and 3rd positions of the quinoxaline ring.

This compound is known to have various biological activities, such as antimicrobial, antifungal, and anticancer properties. However, its use in medical treatments is not widespread due to potential toxicity and lack of comprehensive studies on its safety and efficacy. As with any chemical compound, it should be handled with care and used only under appropriate laboratory conditions.

NADPH Dehydrogenase (also known as Nicotinamide Adenine Dinucleotide Phosphate Hydrogen Dehydrogenase) is an enzyme that plays a crucial role in the electron transport chain within the mitochondria of cells. It catalyzes the oxidation of NADPH to NADP+, which is a vital step in the process of cellular respiration where energy is produced in the form of ATP (Adenosine Triphosphate).

There are multiple forms of this enzyme, including both membrane-bound and soluble varieties. The membrane-bound NADPH Dehydrogenase is a complex I protein found in the inner mitochondrial membrane, while the soluble form is located in the cytosol.

Mutations in genes encoding for this enzyme can lead to various medical conditions, such as mitochondrial disorders and neurological diseases.

Quinoxalines are not a medical term, but rather an organic chemical compound. They are a class of heterocyclic aromatic compounds made up of a benzene ring fused to a pyrazine ring. Quinoxalines have no specific medical relevance, but some of their derivatives have been synthesized and used in medicinal chemistry as antibacterial, antifungal, and antiviral agents. They are also used in the production of dyes and pigments.

Astrocytes are a type of star-shaped glial cell found in the central nervous system (CNS), including the brain and spinal cord. They play crucial roles in supporting and maintaining the health and function of neurons, which are the primary cells responsible for transmitting information in the CNS.

Some of the essential functions of astrocytes include:

1. Supporting neuronal structure and function: Astrocytes provide structural support to neurons by ensheathing them and maintaining the integrity of the blood-brain barrier, which helps regulate the entry and exit of substances into the CNS.
2. Regulating neurotransmitter levels: Astrocytes help control the levels of neurotransmitters in the synaptic cleft (the space between two neurons) by taking up excess neurotransmitters and breaking them down, thus preventing excessive or prolonged activation of neuronal receptors.
3. Providing nutrients to neurons: Astrocytes help supply energy metabolites, such as lactate, to neurons, which are essential for their survival and function.
4. Modulating synaptic activity: Through the release of various signaling molecules, astrocytes can modulate synaptic strength and plasticity, contributing to learning and memory processes.
5. Participating in immune responses: Astrocytes can respond to CNS injuries or infections by releasing pro-inflammatory cytokines and chemokines, which help recruit immune cells to the site of injury or infection.
6. Promoting neuronal survival and repair: In response to injury or disease, astrocytes can become reactive and undergo morphological changes that aid in forming a glial scar, which helps contain damage and promote tissue repair. Additionally, they release growth factors and other molecules that support the survival and regeneration of injured neurons.

Dysfunction or damage to astrocytes has been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

The limbic system is a complex set of structures in the brain that includes the hippocampus, amygdala, fornix, cingulate gyrus, and other nearby areas. It's associated with emotional responses, instinctual behaviors, motivation, long-term memory formation, and olfaction (smell). The limbic system is also involved in the modulation of visceral functions and drives, such as hunger, thirst, and sexual drive.

The structures within the limbic system communicate with each other and with other parts of the brain, particularly the hypothalamus and the cortex, to regulate various physiological and psychological processes. Dysfunctions in the limbic system can lead to a range of neurological and psychiatric conditions, including depression, anxiety disorders, post-traumatic stress disorder (PTSD), and certain types of memory impairment.

... taking prekainic acid to the final kainic acid. KabC was also able to produce another kainic acid isomer, kainic acid lactone. ... Kainic acid, or kainate, is an acid that naturally occurs in some seaweed. Kainic acid is a potent neuroexcitatory amino acid ... Kainic acid is commonly injected into laboratory animal models to study the effects of experimental ablation. Kainic acid is a ... In addition to inducing seizures, kainic acid is excitotoxic and epileptogenic. Kainic acid induces seizures via activation of ...
AMPA Domoic acid Kainic acid NMDA Quinolinic acid Quisqualic acid Tetrazolylglycine Acetylcholine receptor agonists are drugs ... For example, kainic acid can lead to status epilepticus in animals as it is a cyclic analog of l-glutamate and an agonist for ... "Kainic Acid - an overview , ScienceDirect Topics". www.sciencedirect.com. Retrieved 2022-01-15. "GABA-A Receptor Antagonists - ... 3-Mercaptopropionic acid Allylglycine Glycine receptor antagonists are drugs which inactivates the glycine receptors. ...
... making it a dicarboxylic acid. It is an inhibitor of the GLT-1 glutamate transporter. Kainic acid Kawahara, K; Hosoya, R; Sato ... Dihydrokainic acid is an organic compound that contains two carboxylic acid functional groups, ... Dicarboxylic acids, Isopropyl compounds, Pyrrolidines, All stub articles, Organic compound stubs). ...
I. Effects of kainic acid-induced lesions". Journal of Neurophysiology. 52 (2): 290-304. doi:10.1152/jn.1984.52.2.290. PMID ...
... may occur with hypoxic-ischemic injury, hypoglycemia, toxins (kainic acid, domoic acid), and viral human ... Lévesque, Maxime; Avoli, Massimo (2013). "The kainic acid model of temporal lobe epilepsy". Neuroscience & Biobehavioral ... Lefebvre, Kathi A.; Robertson, Alison (2010). "Domoic acid and human exposure risks: A review". Toxicon. 56 (2): 218-230. doi: ... 1990). "Neurologic Sequelae of Domoic Acid Intoxication Due to the Ingestion of Contaminated Mussels". New England Journal of ...
Coyle, Joseph T.; Schwarcz, Robert (1976). "Lesion of Striatal Neurons with Kainic Acid Provides a Model for Huntington's ... Nadler; Victor, J.; Perry, Bruce W.; Cotman, Carl W. (1978). "Intraventricular Kainic Acid Preferentially Destroys Hippocampal ... Caramboxin is a new nonpeptide amino acid toxin that stimulate the glutamate receptors in neurons. Caramboxin is an agonist of ... It is known that the mercuric ion inhibits amino acid (AA) and glutamate (Glu) transport, potentially leading to excitotoxic ...
Jakuš J., Stránsky A., Poliaèek I., Baráni H., Bošelová ¼.: Kainic acid lesion to the Lateral tegmental field of medulla. ...
They have five subunits, divided into two main families: GluK1,2, and GluK5,6,7. An endogenous ligand, either kainic acid or ... It is well characterized that injection of kainic acid can induce seizures, including temporal lobe epilepsy months after ... Consistent with these findings, transgenic mice with knocked out GluK1 have reduced seizures after treatment with kainic acid. ... Bunch, Lennart; Krogsgaard‐Larsen, Povl (2009). "Subtype selective kainic acid receptor agonists: Discovery and approaches to ...
"Huprine X Attenuates The Neurotoxicity Induced by Kainic Acid, Especially Brain Inflammation". Basic & Clinical Pharmacology & ...
Kainic acid as a tool for the study of temporal lobe epilepsy". Life Sci. 29 (20): 2031-42. doi:10.1016/0024-3205(81)90659-7. ... Ben-Ari Y (February 1985). "Limbic seizure and brain damage produced by kainic acid: mechanisms and relevance to human temporal ... RNA editing of the Q/R site can affect inhibition of the channel by membrane fatty acids such as arachidonic acid and ... "Amino acid substitutions in the pore helix of GluR6 control inhibition by membrane fatty acids". J. Gen. Physiol. 132 (1): 85- ...
Stafstrom, Carl E.; Thompson, James L.; Holmes, Gregory L. (February 1992). "Kainic acid seizures in the developing brain: ... SEIZURE RISK DUE TO DECREASED INHIBITION: Gamma-butyric acid (GABA) is the main inhibitory neurotransmitter in adult humans. ... brain is hyperexcitable due to excess in excitatory glutaminergic neurons and immaturity of inhibitory gamma-amino butyric acid ...
Ed., 46, 5734-5736 (2007). A Practical Synthesis of (-)-Kainic Acid, S. Takita, S. Yokoshima, and T. Fukuyama, Org. Lett., 13, ...
... (DA) is a kainic acid-type neurotoxin that causes amnesic shellfish poisoning (ASP). It is produced by algae and ... Domoic acid is a structural analog of kainic acid, proline, and endogenous excitatory neurotransmitter glutamate. Ohfune and ... In addition domoic acid was used to poison a witness in the Elementary Season 1 Episode 13: "The Red Team". Domoic acid ... Domoic acid is an excitatory amino acid analogue of glutamate; a neurotransmitter in the brain that activates glutamate ...
Similar results are obtained after injection of kainic acid, an analog of glutamic acid which causes a severe neurodegenerative ... Tg mice treated with kainic acid show a significant reduction of inflammatory responses and a much stronger protection against ... Other ApoD ligands include E-3-methyl-2-hexenoïc acid, a scent molecule present in body odor secretions; retinoic acid, which ... ApoD is 169 amino acids long, including a secretion peptide signal of 20 amino acids. It contains two glycosylation sites ( ...
Part 10: A Concise Synthesis of (−)-Kainic Acid via Sulfanyl Radical Addition-Cyclization-Elimination Reaction". Tetrahedron. ... α-kainic acid, asperparalines, and alkaloids such as narciclasine and lycoricidine. Intramolecular thiol-ene reactions provide ...
5-Iodowillardiine ATPA Domoic acid Glutamic acid (glutamate) - the endogenous agonist Kainic acid - the agonist after which the ... The convulsant kainic acid induces seizures, in part, by activation of kainate receptors containing the GluK2 subunit and also ... Kainate receptors, or kainic acid receptors (KARs), are ionotropic receptors that respond to the neurotransmitter glutamate. ... receptor is named LY-339,434 SYM-2081 CNQX DNQX Ethanol - non-selective NS102 Kynurenic acid - endogenous ligand Tezampanel - ...
Besharse, Joseph C.; Spratt, Gwendolyn; Forestner, Donna M. (8 September 1986). "Light-evoked and kainic-acid-induced disc ...
Kainic acid is an example of an excitatory amino acid used in this type of lesion. One crucial benefit to this lesion is its ... An excitotoxic lesion is the process of an excitatory amino acid being injected into the brain using a cannula. The amino acid ...
Coyle JT, Schwarcz R. Lesion of striatal neurons with kainic acid provides a model for Huntington's chorea. Nature. 1976 Sep; ...
Godaux E, Mettens P, Cheron G (1993). "Differential effect of injections of kainic acid into the prepositus and the vestibular ... Cheron, G.; Godaux, E. (1 December 1987). "Disabling of the oculomotor neural integrator by kainic acid injections in the ... Cheron G, Godaux E (1987). "Disabling of the oculomotor neural integrator by kainic acid injections in the prepositus- ... Cheron G, Godaux E (1987). "Disabling of the oculomotor neural integrator by kainic acid injections in the prepositus- ...
Kainic acid, used to model TLE and related scleroses, affects primarily the mossy fiber synapses in CA3. It is thought that at ... These receptors are most dense in sectors CA3 and CA2 of the hippocampus, where nanomolar (nM) concentrations of kainic acid ...
Hong YM, Jo DG, Lee MC, Kim SY, Jung YK (2003). "Reduced expression of calsenilin/DREAM/KChIP3 in the brains of kainic acid- ...
Selectracetam has been demonstrated to not significantly affect currents gated by NMDA, AMPA, GABA, glycine, or kainic acid. ... The main metabolic mechanism is the hydrolysis of an acetamide to a carboxylic acid. Seletracetam exhibits first-order mono- ... is excreted in the form of an inactive carboxylic acid metabolite. ...
... reduces reactive gliosis and protects hippocampal hilar neurons from kainic acid excitotoxicity". Journal of Neuroscience ...
... and kainic acid. However, this denatured venom did not inhibit seizures induced by pentylenetetrazole. These findings imply ... implying the presence of free amino acids. These free amino acids would need to be further studied to determine their exact ...
It has also been shown in different animal models, such as the kainic acid model, pilocarpine model, and kindling model. But ... "Abnormalities of granule cell dendritic structure are a prominent feature of the intrahippocampal kainic acid model of epilepsy ...
... inhibited seizures evoked by bicuculline, pentylenetetrazole, and kainic acid as well as increasing the latency of ... erythravine prevented death in all the animals tested with the four convulsants except a few of those treated with kainic acid ...
... such as kainic acid treated animals. Fluoro-jade-stained tissue can be visualized under an epifluorescent microscope using a ... terepthalic acid, and (3) disodium 2,5-bis(6-hydroxy-3-oxo-3H-xanthen-9yl)terepthalic acid. All three fluoro-jade species have ... Olmos's cupric-staining methodologies in a variety of neurotoxic models of neurodegeneration such as injection of kainic acid, ... fuchsine acid, could successfully bind to damaged neurons after a hyperglycemic insult presumably by the same electrostatic ...
In certain cases, seizures tend to appear to originate from the claustrum when they are involved in early kainic acid induced ...
... administration have shown a neuroprotective effect on hippocampal neurons in seizure models induced by kainic acid. The proper ...
... taking prekainic acid to the final kainic acid. KabC was also able to produce another kainic acid isomer, kainic acid lactone. ... Kainic acid, or kainate, is an acid that naturally occurs in some seaweed. Kainic acid is a potent neuroexcitatory amino acid ... Kainic acid is commonly injected into laboratory animal models to study the effects of experimental ablation. Kainic acid is a ... In addition to inducing seizures, kainic acid is excitotoxic and epileptogenic. Kainic acid induces seizures via activation of ...
Ameliorative influence of cnestis ferruginea vahl ex DC (connaraceae) root extract on kainic acid-induced temporal lobe ... Ameliorative influence of cnestis ferruginea vahl ex DC (connaraceae) root extract on kainic acid-induced temporal lobe ... Ameliorative influence of cnestis ferruginea vahl ex DC (connaraceae) root extract on kainic acid-induced temporal lobe ...
... α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), and kainic acid (KA) receptors, overexcites neurons and triggers ... PKD1 protects against kainic acid-induced excitotoxicity. To investigate PKD1 neuroprotection in vivo, we selected a model of ... Treatment with kainic acid. Twelve days after lentiviral CA1 intracerebral injection, rats were treated with a single ... Wang, Q., Yu, S., Simonyi, A., Sun, G. Y. & Sun, A. Y. Kainic acid-mediated excitotoxicity as a model for neurodegeneration. ...
... kainic acid excitotoxicity-induced spinal cord injury paraplegia in Sprague-Dawley rats; Anjum A, Cheah YJ, Yazid MD, et al. ... following intra-spinal kainic acid administration at desired location. The dose, rate and technique to administer kainic acid ... CONCLUSIONS: Kainic acid intra-spinal injection at the concentration of 0.05 mM, and rate 10 µL/min, is an effective method ... The kainic acid (KA) excitotoxicity model is a convenient, low-cost, and highly reproducible animal model of SCI in the ...
Kainic acid, prototypic kainate receptor agonist (ab120100) Specific References (63) Description:. Prototypic kainate receptor ... Quisqualic acid, group I mGlu agonist. AMPA agonist. (ab120010) Specific References (1) ...
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid * cyclothiazide * Kainic Acid ... In this study, the effects of 1-BCP on excitatory amino acid agonist-induced [3H]NE release in rat hippocampal slices were ...
Kainic Acid Grants and funding * EY-00824/EY/NEI NIH HHS/United States ...
Kainic acid injection into the ventral hippocampus induced status epilepticus. RESULTS: Seizures caused hypertension, ... Brainstem activity, apnea, and death during seizures induced by intrahippocampal kainic acid in anaesthetized rats. ... Kainic acid injection into the ventral hippocampus induced status epilepticus. RESULTS: Seizures caused hypertension, ... Brainstem activity, apnea, and death during seizures induced by intrahippocampal kainic acid in anaesthetized rats. ...
1978) Excitatory amino acids. in Kainic acid as a tool in neurobiology, eds McGeer EG, Olney JW, McGeer PL (Raven, New York), ... 1983) Kainic acid selectively stimulates the release of endogenous excitatory acidic amino acids. J Pharmacol Exp Ther 225:399- ... Effect of IL-1β and/or IL-1Ra on kainic acid-induced EEG seizures. Figure 8 shows the effect of 0.1 and 1.0 ng of (hr)IL-1β and ... 1998) Kainic acid induced expression of interleukin-1 receptor antagonist mRNA in the rat brain. Mol Brain Res 58:195-208. ...
Dive into the research topics of Studies of effects of kainic acid lesions in the dorsal lateral geniculate nucleus of rat. ... Studies of effects of kainic acid lesions in the dorsal lateral geniculate nucleus of rat. ...
Either kainic acid (KA; 0.3 μg in 0.5 μl PBS) or vehicle (0.5 μl PBS) was infused into the right amygdala at the rate of 0.11 ... Surgery and amygdala kainic acid microinfusion.. Adult male and female mice (20-30 g) were anesthetized and placed in a ... hippocampal CA3-predominant damage and short latency epileptogenesis after intra-amygdala microinjection of kainic acid in mice ...
keywords = "Hippocampus, Kainic acid, NFκB, Neurotoxicity, TNF-α",. author = "Zhang, {Xing Mei} and Zheng, {Xiang Yu} and ... Possible protecting role of TNF-α in kainic acid-induced neurotoxicity via down-regulation of NFκB signaling pathway. Current ... Possible protecting role of TNF-α in kainic acid-induced neurotoxicity via down-regulation of NFκB signaling pathway. In: ... Possible protecting role of TNF-α in kainic acid-induced neurotoxicity via down-regulation of NFκB signaling pathway. / Zhang, ...
This transformation wase utilized successfully in a total synthesis of kainic acid (Scheme 9). This beautiful example shows ... α-kainic acid. Angew. Chem. Int. Ed. Engl. 2011, 123, 6494-6498. [Google Scholar] [CrossRef] ... Brichacek, M.; Lee, D.; Njardarson, J.T. Lewis Acid catalyzed [1,3]-sigmatropic rearrangement of vinylaziridines. Org. Lett. ...
... kainic Acid; Kir4.1, inwardly rectifying potassium; MCL, molecular cell layer; MR, magnetic resonance; NeuN, neuronal nuclei; ... ethylene glycol tetraacetic acid), 1 mM EDTA (ethylenediaminetetraacetic acid), and protease inhibitor (Roche Custom Biotech, ... Sections were deparaffinized, followed by antigen-retrieval (0.01 M citric acid in a water bath of 95°C for 20 min, followed by ... gamma-aminobutyric acid type A; GCL, granular cell layer; GFAP, glial fibrillary acidic protein; HS, hippocampal sclerosis; KA ...
Glutamic Acid/pharmacology. *Hippocampus/cytology. *Kainic Acid/toxicity. *Membrane Proteins/genetics. *Membrane Proteins/ ... Variant, nucleic acid level: c.1907C,T. *Variant, amino acid level, predicted: p.Pro636Leu. Check this variant: LUMC Mutalyzer ... Variant, nucleic acid level: c.433_436delinsGTTG. *Variant, amino acid level, predicted: p.Ile145_Met146delinsValVal. Check ... Variant, amino acid level, predicted: p.Lys670_Met671delinsAsnLeu (K670N/M671L). Check this variant: LUMC Mutalyzer. ...
Domoic acid binds to and stimulates the kainic acid glutamate receptor, [4] which allows sodium influx and a small amount of ... Domoic acid has been associated with necrosis of the glutamate-rich hippocampus and amygdala in autopsied cases. Domoic acid is ... Common marine HAB toxins found in shellfish include brevetoxins, azaspiracid, domoic acid, okadic acid, saxitoxin. [1] ... Prenatal domoic acid exposure disrupts mouse pro-social behavior and functional connectivity MRI. Behav Brain Res. 2016 Jul 15 ...
P38 Regulates Kainic Acid-Induced Seizure and Neuronal Firing via Kv4.2 Phosphorylation by Jia-hua Hu ... Using a combination of biochemical, single-cell electrophysiology, and in vivo seizure techniques, we show that kainic acid- ... CA9 silencing also downregulated amino acid transporters, leading to reduced cellular amino acids. Collectively, our data show ... encoding 890 amino acids, and an ORF of 1935 bp, encoding 644 amino acids. Both the ToTLR5s possess representative TLR domains ...
Enhancing brain repair potential in kainic acid-degenerated hippocampus by pluripotency inducers. *O1-J-1-4 ...
After baseline EEG recordings, a cannula was inserted to inject kainic acid (0.3 µg/0.2 μl in phosphate-buffered saline; PBS) ... Nucleic Acids Res 2020, 48:D498-D503.. 40.Kanehisa M, Goto S: KEGG: kyoto encyclopedia of genes and genomes. Nucleic Acids Res ... Status epilepticus after intraamygdala microinjection of kainic acid was similar between wildtype, miR-22+/- and miR-22-/- mice ... While we did not observe differences in status epilepticus in the intraamygdala kainic acid model, miR-22-deficient mice may ...
Parenterally administered kainic acid induces a persistent hyperalgesia in the mouse and rat by. Giovengo SL, Kitto KF, Kurtz ... Kainic acid injected subcutaneously in the back of mice decreased response latencies in the hot plate and tail flick assays, ... Nociceptive primary afferent C-fibers express a subset of glutamate receptors that are sensitive to kainic acid. Thus, we ... When injected intrathecally (i.t.), kainic acid itself failed to induce hyperalgesia and AMPA/KA antagonists given i.t. also ...
Kainic Acid, NMDA and Bicuculline Induce Elevation in Concentrations of Glutathione and Amino Acids in Vivo: Biomarkers for ...
The brains of mice lacking Sirt3 experience more cell death (blue) upon excitotoxic treatment with glutamate, kainic acid, and ... Chemical modulation of chaperone-mediated autophagy by retinoic acid derivatives.. Nat Chem Biol. 2013 Jun;9(6):374-82. doi: ...
Journal Article] Limb-clasping, cognitive deficit and increased vulnerability to kainic acid - induced seizures in neuronal GPI ... Presentation] Limb-clasping, cognitive deficit and increased vulnerability to kainic acid-induced seizures in neuronal ...
Role of gamma-aminobutyric acid B (GABA B) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus ... Kainic acid (KA) is well-known as an excitatory, neurotoxic substance. In mice, KA administered intracerebroventricularly (i.c. ... delta in microglia following kainic acid-induced seizures Eun SY, Kim EH, Kang KS, Kim HJ, Jo SA, Kim SJ, Jo SH, Kim SJ, ...
Blueberry polyphenols attenuate kainic acid-induced decrements in cognition and alter inflammatory gene expression in rat ... The reason for the similarity in behavioral deficits between aged and kainic acid-injected rats, as mentioned above, might be ... Furthermore, rats fed with the blueberry diet prior to kainic acid injection exhibited less activation of the inflammatory ... 2008) reported that blueberry polyphenols attenuated kainic acid-induced learning impairments in rats, which were similar to ...
Kainic acid lesions were also produced in either hippocampal field 1 day after training and retention measured 8 days later. ...
Calretinin/PSA-NCAM immunoreactive granule cells after hippocampal damage produced by kainic acid and DEDTC treatment in mouse. ... Castillo-Gómez E; Varea E; Blasco-Ibáñez JM; Crespo C; Nacher J. (2011) Polysialic Acid is required for dopamine d2 receptor- ... Effects of Chronic Dopamine D2R Agonist Treatment and Polysialic Acid Depletion on Dendritic Spine Density and Excitatory ...
Everolimus is better than rapamycin in attenuating neuroinflammation in kainic acid-induced seizures. J. Neuroinflammation, ... Jiang, P.; Guo, Y.; Dang, R.; Yang, M.; Liao, D.; Li, H.; Sun, Z.; Feng, Q.; Xu, P. Salvianolic acid B protects against ... Yang, Z.; Huang, J.; Geng, J.; Nair, U.; Klionsky, D.J. Atg22 recycles amino acids to link the degradative and recycling ... Moharregh-Khiabani, D.; Linker, R.A.; Gold, R.; Stangel, M. Fumaric Acid and its esters: an emerging treatment for multiple ...
It is an analogue of kainic acid and a neurotoxin which causes amnesic shellfish poisoning (ASP).. ... domoic acid results in increased expression of GCLC mRNA; domoic acid results in increased expression of GCLC protein. CTD. ... domoic acid results in increased expression of GCLM mRNA; domoic acid results in increased expression of GCLM protein. GCLM ... domoic acid results in increased expression of WDR35 mRNA; domoic acid results in increased expression of WDR35 protein. 2,3- ...
  • Also, infusion with kainic acid in the hippocampus of animals results in major damage of pyramidal neurons and subsequent seizure activity. (wikipedia.org)
  • Kainic acid injection into the ventral hippocampus induced status epilepticus. (ox.ac.uk)
  • Using immunocytochemistry and ELISA, we investigated the production of interleukin (IL)-1β in the rat hippocampus after focal application of kainic acid inducing electroencephalographic (EEG) seizures and CA3 neuronal cell loss. (jneurosci.org)
  • Domoic acid has been associated with necrosis of the glutamate-rich hippocampus and amygdala in autopsied cases. (medscape.com)
  • miR-22-3p (hereafter miR-22), a conserved miRNA that is expressed throughout the body, including the brain [ 14 , 15 ], was previously identified among upregulated miRNAs within the mouse hippocampus contralateral to the epileptogenic zone in the intraamygdala kainic acid model of status epilepticus [ 16 ]. (researchsquare.com)
  • The third was an investigation of the excitatory amino acid receptors responsible for epileptiform bursting activity in 2 animal models of epilepsy: a chronic model of temporal lobe epilepsy, involved prior lesioning of the hippocampus with kainic acid, and an acute model which involved application of the GABA-A receptor antagonist, bicuculline. (soton.ac.uk)
  • Kainic acid is a potent central nervous system excitant that is used in epilepsy research to induce seizures in experimental animals, at a typical dose of 10-30 mg/kg in mice. (wikipedia.org)
  • In addition to inducing seizures, kainic acid is excitotoxic and epileptogenic. (wikipedia.org)
  • Kainic acid induces seizures via activation of kainate receptors containing the GluK2 subunit and also through activation of AMPA receptors, for which it serves as a partial agonist. (wikipedia.org)
  • Brainstem activity, apnea, and death during seizures induced by intrahippocampal kainic acid in anaesthetized rats. (ox.ac.uk)
  • Journal Article] Limb-clasping, cognitive deficit and increased vulnerability to kainic acid - induced seizures in neuronal GPI anchor deficiency mouse models. (nii.ac.jp)
  • Differential 24h responsiveness of Prox1-expressing precursor cells in adult hippocampal neurogenesis to physical activity, environmental enrichment, and kainic acid-induced seizures. (mpg.de)
  • Mice homozygous for a conditional allele activated in the brain exhibit reduced fertility, infrequent spontaneous seizures, increased susceptibility to kainic acid-induced seizures and lethality, and increased neuronal excitation. (jax.org)
  • Kainic acid is a potent neuroexcitatory amino acid agonist that acts by activating receptors for glutamate, the principal excitatory neurotransmitter in the central nervous system. (wikipedia.org)
  • Kainic acid is an agonist for kainate receptors, a type of ionotropic glutamate receptor. (wikipedia.org)
  • Kainic acid is a direct agonist of the glutamic kainate receptors and large doses of concentrated solutions produce immediate neuronal death by overstimulating neurons to death. (wikipedia.org)
  • N ociceptive primary afferent C-fibers express a subset of glutamate receptors that are sensitive to kainic acid. (biopsychiatry.com)
  • Excitotoxicity refers to the neurotoxic effect of excitatory amino acids in the presence of excessive activation of postsynaptic receptors. (medscape.com)
  • In this study, the effects of 1-BCP on excitatory amino acid agonist-induced [3H]NE release in rat hippocampal slices were determined. (nih.gov)
  • We have shown previously, that mice lacking tumor necrosis factor-α (TNF-α) receptor 1 (TNFR1) exhibit greater hippocampal neurodegeneration, suggesting that TNFR1 may be protective in kainic acid (KA)-induced neurotoxicity. (uaeu.ac.ae)
  • Kainic acid lesions were also produced in either hippocampal field 1 day after training and retention measured 8 days later. (karger.com)
  • We designed this study to investigate the potential of extract of Asparagus racemosus against kainic acid (KA)-induced hippocampal and striatal neuronal damage. (raysahelian.com)
  • The excitotoxic lesion in brain was produced by intra-hippocampal and intra-striatal injections of kainic acid to ketamine and xylazine anesthetized mice. (raysahelian.com)
  • In 2019, Chekan et al were able to use bioinformatic tools to look for domoic acid gene homologs in the seaweed Digenea simplex. (wikipedia.org)
  • neuroscience research neurodegenerative agent modeling of epilepsy modeling of Alzheimer's disease Dihydrokainic acid Domoic acid Kainate receptor Carlson NR (2013). (wikipedia.org)
  • Domoic acid (DA) is structurally similar to the excitatory neurotransmitter glutamate. (medscape.com)
  • Domoic acid is produced by the diatom Nitzschia pungens . (medscape.com)
  • Domoic acid (Cat. (tocris.com)
  • Domoic acid is a kainate receptor agonist. (tocris.com)
  • Be the first to review Domoic acid and earn rewards! (tocris.com)
  • Have you used Domoic acid? (tocris.com)
  • When administered i.p., 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an (R,S)-alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid HBr/kainate (AMPA/KA) antagonist, completely blocked hyperalgesia. (biopsychiatry.com)
  • When injected intrathecally (i.t.), kainic acid itself failed to induce hyperalgesia and AMPA/KA antagonists given i.t. also failed to attenuate the hyperalgesic effect of kainic acid administered i.p., indicating that the spinal cord is not the primary site of action. (biopsychiatry.com)
  • Thus, in large, concentrated doses kainic acid can be considered a neurotoxin, and in small doses of dilute solution kainic acid will chemically stimulate neurons. (wikipedia.org)
  • Intrastriatal injections of quinolinic acid, an N -methyl-D-aspartate (NMDA) receptor agonist, selectively affect medium-sized GABA-ergic spiny projection neurons, sparing the striatal interneurons and closely mimicking the neuropathology seen in HD. (medscape.com)
  • The glutamate receptor agonist kainic acid [21] and the cholinergic agonist pilocarpine [22] are commonly used in SE models. (jle.com)
  • Intrastriatal injections of kainic acid, an agonist of a subtype of glutamate receptor, produce lesions similar to those seen in HD. (medscape.com)
  • Kainic acid (KA) is well-known as an excitatory, neurotoxic substance. (koreamed.org)
  • Excitatory Amino Acids and Synaptic Plasticity. (tocris.com)
  • Therefore, the most effective ablation studies are performed in comparison to a sham lesion that duplicates all the steps of producing a brain lesion except the one that actually causes the brain damage, that is, injection of kainic acid or administration of an electrical shock. (wikipedia.org)
  • CONCLUSIONS: Kainic acid intra-spinal injection at the concentration of 0.05 mM, and rate 10 µL/min, is an effective method create spinal injury in rats, however more potent concentrations of kainic acid need to be studied in order to create severe spinal injuries. (afpm.org.my)
  • Intraperitoneal (i.p.) injection of kainic acid induced a persistent thermal hyperalgesia, when tested using the hot plate (mice) and tail flick (mice and rats) assays, and mechanical hyperalgesia when tested using von Frey monofilaments (rats), but had no effect on acetic acid-induced chemical nociception (mice). (biopsychiatry.com)
  • Kainic acid injected subcutaneously in the back of mice decreased response latencies in the hot plate and tail flick assays, indicating that hyperalgesia is achieved by a variety of parenteral routes of injection. (biopsychiatry.com)
  • Kainic acid, or kainate, is an acid that naturally occurs in some seaweed. (wikipedia.org)
  • The dose, rate and technique to administer kainic acid were explained extensively to reflect a successful paraplegia and spinal cord injury in rats. (afpm.org.my)
  • Okadaic acid binds to intestinal epithelial cells and increases their permeability. (medscape.com)
  • Histological evaluation of rat spinal cord and dorsal root ganglia revealed no neurodegenerative changes 24 h after kainic acid. (biopsychiatry.com)
  • The neuroprotective effects of berry fruits on neurodegenerative diseases are related to phytochemicals such as anthocyanin, caffeic acid, catechin, quercetin, kaempferol and tannin. (lww.com)
  • Data from in vitro and animal studies suggest that among the sources of antioxidants, phytochemicals in berry fruits ( e.g. , anthocyanin and caffeic acid) have a beneficial role in brain aging and neurodegenerative disorders because of their anti-oxidative, anti-inflammatory, anti-viral and anti-proliferative properties (Youdim et al. (lww.com)
  • Kainic acid is utilised in primary neuronal cell cultures and in the acute brain slice preparation to study the physiological effect of excitotoxicity and assess the neuroprotective capabilities of potential therapeutics. (wikipedia.org)
  • The kainic acid (KA) excitotoxicity model is a convenient, low-cost, and highly reproducible animal model of SCI in the laboratory. (afpm.org.my)
  • It is an analogue of kainic acid and a neurotoxin which causes amnesic shellfish poisoning (ASP). (mcw.edu)
  • Ameliorative influence of cnestis ferruginea vahl ex DC (connaraceae) root extract on kainic acid-induced temporal lobe epilepsy in mice: Role of oxidative stress and neuroinflammation. (iasp-pain.org)
  • In this protocol, detailed description of a dorsal laminectomy was explained to expose the spinal cord, following intra-spinal kainic acid administration at desired location. (afpm.org.my)
  • Mice lacking miR-22 displayed normal behaviour and brain structure and developed similar status epilepticus after intraamygdala kainic acid compared to wildtype animals. (researchsquare.com)
  • The toxins responsible for most shellfish poisonings are water-soluble, are heat and acid-stable, and are not inactivated by ordinary cooking methods. (medscape.com)
  • Kainic acid is commonly injected into laboratory animal models to study the effects of experimental ablation. (wikipedia.org)
  • Supply shortages beginning in 2000 have caused the cost of kainic acid to rise significantly. (wikipedia.org)
  • The basic impactor approximately cost between 10,000 and 20,000 USD, while the kainic acid only cost between 300 and 500 USD, which is quite cheap as compared to traditional SCI method. (afpm.org.my)
  • Therefore, chemical stimulation by kainic acid is more localized than electrical stimulation. (wikipedia.org)
  • The first step of the pathway involves the N-prenyltransferase, KabA, which allows for the prenylation of L-glutamic acid with dimethylallyl pyrophosphate (DMAPP) to form the intermediate N-dimethylallyl-l-glutamic acid (prekainic acid). (wikipedia.org)