Muscimol
GABA Agonists
Receptors, GABA-A
Bicuculline
GABA Antagonists
Baclofen
Microinjections
Receptors, GABA
Cerebellar Nuclei
Flunitrazepam
Picrotoxin
GABA-A Receptor Antagonists
Receptors, GABA-B
Nipecotic Acids
Oxazoles
Medulla Oblongata
GABA Agents
Rats, Sprague-Dawley
Pons
Rats, Long-Evans
Secobarbital
Pentobarbital
Isoxazoles
Diazepam
Chlormethiazole
Neurite outgrowth-regulating properties of GABA and the effect of serum on mouse spinal cord neurons in culture. (1/921)
Time-lapse photography was used to examine the effects of gamma-aminobutyric acid (GABA) on the outgrowth and motility of neurites in cultures from mouse spinal cord. GABA at concentrations of 100, 10 and 1 microM caused significant inhibition of neurite outgrowth and the motility of growth cones was significantly reduced by treatment with 100 and 10 microM GABA. This effect was mimicked by the GABA(B) receptor agonist baclofen, whereas the GABA(A) receptor agonist muscimol had no effect. The effect of GABA on outgrowth and motility seems to be dependent on the type of serum employed. The results reported here were obtained only when heat-inactivated serum was used and not when non heat-inactivated serum was added to the culture medium. They suggest that GABA has a role in the regulation of process outgrowth within the embryonic mouse spinal cord. (+info)Corticofugal amplification of facilitative auditory responses of subcortical combination-sensitive neurons in the mustached bat. (2/921)
Recent studies on the bat's auditory system indicate that the corticofugal system mediates a highly focused positive feedback to physiologically "matched" subcortical neurons, and widespread lateral inhibition to physiologically "unmatched" subcortical neurons, to adjust and improve information processing. These findings have solved the controversy in physiological data, accumulated since 1962, of corticofugal effects on subcortical auditory neurons: inhibitory, excitatory, or both (an inhibitory effect is much more frequent than an excitatory effect). In the mustached bat, Pteronotus parnellii parnellii, the inferior colliculus, medial geniculate body, and auditory cortex each have "FM-FM" neurons, which are "combination-sensitive" and are tuned to specific time delays (echo delays) of echo FM components from the FM components of an emitted biosonar pulse. FM-FM neurons are more complex in response properties than cortical neurons which primarily respond to single tones. In the present study, we found that inactivation of the entire FM-FM area in the cortex, including neurons both physiologically matched and unmatched with subcortical FM-FM neurons, on the average reduced the facilitative responses to paired FM sounds by 82% for thalamic FM-FM neurons and by 66% for collicular FM-FM neurons. The corticofugal influence on the facilitative responses of subcortical combination-sensitive neurons is much larger than that on the excitatory responses of subcortical neurons primarily responding to single tones. Therefore we propose the hypothesis that, in general, the processing of complex sounds by combination-sensitive neurons more heavily depends on the corticofugal system than that by single-tone sensitive neurons. (+info)Selective pruning of more active afferents when cat visual cortex is pharmacologically inhibited. (3/921)
Activity-dependent competition is thought to guide the normal development of specific patterns of neural connections. Such competition generally favors more active inputs, making them larger and stronger, while less active inputs become smaller and weaker. We pharmacologically inhibited the activity of visual cortical cells and measured the three-dimensional structure of inputs serving the two eyes when one eye was occluded. The more active inputs serving the open eye actually became smaller than the deprived inputs from the occluded eye, which were similar to those in normal animals. These findings demonstrate in vivo that it is not the amount of afferent activity but the correlation between cortical and afferent activity that regulates the growth or retraction of these inputs. (+info)Cholinergic and GABAergic regulation of nitric oxide synthesis in the guinea pig ileum. (4/921)
Nitric oxide (NO) synthesis was examined in intact longitudinal muscle-myenteric plexus preparations of the guinea pig ileum by determining the formation of [3H]citrulline during incubation with [3H]arginine. Spontaneous [3H]citrulline production after 30 min was 80-90 dpm/mg, which constituted approximately 1% of the tissue radioactivity. Electrical stimulation (10 Hz) led to a threefold increase in [3H]citrulline formation. Removal of calcium from the medium or addition of NG-nitro-L-arginine strongly inhibited both spontaneous and electrically induced production of [3H]citrulline. TTX reduced the electrically induced but not spontaneous [3H]citrulline formation. The electrically induced formation of [3H]citrulline was diminished by (+)-tubocurarine and mecamylamine and enhanced by scopolamine, which suggests that endogenous ACh inhibits, via muscarinic receptors, and stimulates, via nicotinic receptors, the NO synthesis in the myenteric plexus. The GABAA receptor agonist muscimol and GABA also reduced the electrically evoked formation of [3H]citrulline, whereas baclofen was without effect. Bicuculline antagonized the inhibitory effect of GABA. It is concluded that nitrergic myenteric neurons are equipped with GABAA receptors, which mediate inhibition of NO synthesis. (+info)RVLM and raphe differentially regulate sympathetic outflows to splanchnic and brown adipose tissue. (5/921)
To determine whether neurons in the rostral raphe pallidus (RPa) specifically control the sympathetic nerve activity to brown adipose tissue (BAT SNA), thereby regulating adipocyte metabolism and BAT thermogenesis, the responses in BAT SNA to disinhibition of RPa neurons and to disinhibition of neurons in the vasomotor region of the rostral ventrolateral medulla (RVLM) were compared with those in splanchnic (Spl) SNA, which primarily regulates visceral vasoconstriction. In urethan-chloralose-anesthetized ventilated rats, both acute hypothermia and microinjection of bicuculline into RPa produced significantly larger increases in BAT SNA (542 and 1,949% of control) than in Spl SNA (19 and 24% of control). The enhanced burst discharge in BAT SNA was not coherent with that in Spl SNA or with the arterial pressure (AP) at any frequency except the central respiratory frequency. Microinjections of bicuculline into RVLM evoked increases in Spl SNA (86% of control) and AP (32 mmHg), but reduced BAT SNA to low, normothermic levels. Microinjections of muscimol into RVLM reduced Spl SNA (-82% of control) and AP (-59 mmHg), but did not prevent the increase in BAT SNA after disinhibition of RPa neurons. These results indicate that the neural networks generating BAT SNA in response to disinhibition of RPa neurons are independent of those generating basal Spl SNA and support a model in which sympathetic outflow to tissues involved in thermoregulation and metabolism is regulated by central pathways, including neurons in RPa, that are distinct from those involved in the sympathetic control of the cardiovascular system. (+info)Effect of reversible inactivation of macaque lateral intraparietal area on visual and memory saccades. (6/921)
Previous studies from our laboratory identified a parietal eye field in the primate lateral intraparietal sulcus, the lateral intraparietal area (area LIP). Here we further explore the role of area LIP in processing saccadic eye movements by observing the effects of reversible inactivation of this area. One to 2 microl of muscimol (8 mg/ml) were injected at locations where saccade-related activities were recorded for each lesion experiment. After the muscimol injection we observed in two macaque monkeys consistent effects on both the metrics and dynamics of saccadic eye movements at many injection sites. These effects usually took place within 10-30 min and disappeared after 5-6 h in most cases and certainly when tested the next day. After muscimol injection memory saccades directed toward the contralesional and upper space became hypometric, and in one monkey those to the ipsilesional space were slightly but significantly hypermetric. In some cases, the scatter of the end points of memory saccades was also increased. On the other hand, the metrics of visual saccades remained relatively intact. Latency for both visual and memory saccades toward the contralesional space was increased and in many cases displayed a higher variance after muscimol lesion. At many injection sites we also observed an increase of latency for visual and memory saccades toward the upper space. The peak velocities for memory saccades toward the contralesional space were decreased after muscimol injection. The peak velocities of visual saccades were not significantly different from those of the controls. The duration of saccadic eye movements either to the ipsilesional or contralesional space remained relatively the same for both visual and memory saccades. Overall these results demonstrated that we were able to selectively inactivate area LIP and observe effects on saccadic eye movements. Together with our previous recording studies these results futher support the view that area LIP plays a direct role in processing incoming sensory information to program saccadic eye movements. The results are consistent with our unit recording data and microstimulation studies, which suggest that area LIP represents contralateral space and also has a bias for the upper visual field. (+info)Reacquisition deficits in prism adaptation after muscimol microinjection into the ventral premotor cortex of monkeys. (7/921)
A small amount of muscimol (1 microl; concentration, 5 microg/microl) was injected into the ventral and dorsal premotor cortex areas (PMv and PMd, respectively) of monkeys, which then were required to perform a visually guided reaching task. For the task, the monkeys were required to reach for a target soon after it was presented on a screen. While performing the task, the monkeys' eyes were covered with left 10 degrees, right 10 degrees, or no wedge prisms, for a block of 50-100 trials. Without the prisms, the monkeys reached the targets accurately. When the prisms were placed, the monkeys initially misreached the targets because the prisms displaced the visual field. Before the muscimol injection, the monkeys adapted to the prisms in 10-20 trials, judging from the horizontal distance between the target location and the point where the monkey touched the screen. After muscimol injection into the PMv, the monkeys lost the ability to readapt and touched the screen closer to the location of the targets as seen through the prisms. This deficit was observed at selective target locations, only when the targets were shifted contralaterally to the injected hemisphere. When muscimol was injected into the PMd, no such deficits were observed. There were no changes in the reaction and movement times induced by muscimol injections in either area. The results suggest that the PMv plays an important role in motor learning, specifically in recalibrating visual and motor coordinates. (+info)Muscimol-induced inactivation of monkey frontal eye field: effects on visually and memory-guided saccades. (8/921)
Muscimol-induced inactivation of the monkey frontal eye field: effects on visually and memory-guided saccades. Although neurophysiological, anatomic, and imaging evidence suggest that the frontal eye field (FEF) participates in the generation of eye movements, chronic lesions of the FEF in both humans and monkeys appear to cause only minor deficits in visually guided saccade generation. Stronger effects are observed when subjects are tested in tasks with more cognitive requirements. We tested oculomotor function after acutely inactivating regions of the FEF to minimize the effects of plasticity and reallocation of function after the loss of the FEF and gain more insight into the FEF contribution to the guidance of eye movements in the intact brain. Inactivation was induced by microinjecting muscimol directly into physiologically defined sites in the FEF of three monkeys. FEF inactivation severely impaired the monkeys' performance of both visually guided and memory-guided saccades. The monkeys initiated fewer saccades to the retinotopic representation of the inactivated FEF site than to any other location in the visual field. The saccades that were initiated had longer latencies, slower velocities, and larger targeting errors than controls. These effects were present both for visually guided and for memory-guided saccades, although the memory-guided saccades were more disrupted. Initially, the effects were restricted spatially, concentrating around the retinotopic representation at the center of the inactivated site, but, during the course of several hours, these effects spread to flanking representations. Predictability of target location and motivation of the monkey also affected saccadic performance. For memory-guided saccades, increases in the time during which the monkey had to remember the spatial location of a target resulted in further decreases in the accuracy of the saccades and in smaller peak velocities, suggesting a progressive loss of the capacity to maintain a representation of target location in relation to the fovea after FEF inactivation. In addition, the monkeys frequently made premature saccades to targets in the hemifield ipsilateral to the injection site when performing the memory task, indicating a deficit in the control of fixation that could be a consequence of an imbalance between ipsilateral and contralateral FEF activity after the injection. There was also a progressive loss of fixation accuracy, and the monkeys tended to restrict spontaneous visual scanning to the ipsilateral hemifield. These results emphasize the strong role of the FEF in the intact monkey in the generation of all voluntary saccadic eye movements, as well as in the control of fixation. (+info)Muscimol is defined as a cyclic psychoactive ingredient found in certain mushrooms, including Amanita muscaria and Amanita pantherina. It acts as a potent agonist at GABA-A receptors, which are involved in inhibitory neurotransmission in the central nervous system. Muscimol can cause symptoms such as altered consciousness, delirium, hallucinations, and seizures. It is used in research but has no medical applications.
GABA (gamma-aminobutyric acid) agonists are substances that bind to and activate GABA receptors in the brain, mimicking the actions of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. These agents can produce various effects such as sedation, anxiolysis, muscle relaxation, and anticonvulsant activity by enhancing the inhibitory tone in the brain. They are used clinically to treat conditions such as anxiety disorders, seizures, and muscle spasticity. Examples of GABA agonists include benzodiazepines, barbiturates, and certain non-benzodiazepine hypnotics.
GABA-A receptor agonists are substances that bind to and activate GABA-A receptors, which are ligand-gated ion channels found in the central nervous system. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the brain, and its activation via GABA-A receptors results in hyperpolarization of neurons and reduced neuronal excitability.
GABA-A receptor agonists can be classified into two categories: GABAergic compounds and non-GABAergic compounds. GABAergic compounds, such as muscimol and isoguvacine, are structurally similar to GABA and directly activate the receptors. Non-GABAergic compounds, on the other hand, include benzodiazepines, barbiturates, and neurosteroids, which allosterically modulate the receptor's affinity for GABA, thereby enhancing its inhibitory effects.
These agents are used in various clinical settings to treat conditions such as anxiety, insomnia, seizures, and muscle spasticity. However, they can also produce adverse effects, including sedation, cognitive impairment, respiratory depression, and physical dependence, particularly when used at high doses or for prolonged periods.
GABA-A receptors are ligand-gated ion channels in the membrane of neuronal cells. They are the primary mediators of fast inhibitory synaptic transmission in the central nervous system. When the neurotransmitter gamma-aminobutyric acid (GABA) binds to these receptors, it opens an ion channel that allows chloride ions to flow into the neuron, resulting in hyperpolarization of the membrane and decreased excitability of the neuron. This inhibitory effect helps to regulate neural activity and maintain a balance between excitation and inhibition in the nervous system. GABA-A receptors are composed of multiple subunits, and the specific combination of subunits can determine the receptor's properties, such as its sensitivity to different drugs or neurotransmitters.
Bicuculline is a pharmacological agent that acts as a competitive antagonist at GABA-A receptors, which are inhibitory neurotransmitter receptors in the central nervous system. By blocking the action of GABA (gamma-aminobutyric acid) at these receptors, bicuculline can increase neuronal excitability and cause convulsions. It is used in research to study the role of GABAergic neurotransmission in various physiological processes and neurological disorders.
Gamma-Aminobutyric Acid (GABA) is a major inhibitory neurotransmitter in the mammalian central nervous system. It plays a crucial role in regulating neuronal excitability and preventing excessive neuronal firing, which helps to maintain neural homeostasis and reduce the risk of seizures. GABA functions by binding to specific receptors (GABA-A, GABA-B, and GABA-C) on the postsynaptic membrane, leading to hyperpolarization of the neuronal membrane and reduced neurotransmitter release from presynaptic terminals.
In addition to its role in the central nervous system, GABA has also been identified as a neurotransmitter in the peripheral nervous system, where it is involved in regulating various physiological processes such as muscle relaxation, hormone secretion, and immune function.
GABA can be synthesized in neurons from glutamate, an excitatory neurotransmitter, through the action of the enzyme glutamic acid decarboxylase (GAD). Once synthesized, GABA is stored in synaptic vesicles and released into the synapse upon neuronal activation. After release, GABA can be taken up by surrounding glial cells or degraded by the enzyme GABA transaminase (GABA-T) into succinic semialdehyde, which is further metabolized to form succinate and enter the Krebs cycle for energy production.
Dysregulation of GABAergic neurotransmission has been implicated in various neurological and psychiatric disorders, including epilepsy, anxiety, depression, and sleep disturbances. Therefore, modulating GABAergic signaling through pharmacological interventions or other therapeutic approaches may offer potential benefits for the treatment of these conditions.
GABA (gamma-aminobutyric acid) antagonists are substances that block the action of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. GABA plays a crucial role in regulating neuronal excitability and reducing the transmission of nerve impulses.
GABA antagonists work by binding to the GABA receptors without activating them, thereby preventing the normal function of GABA and increasing neuronal activity. These agents can cause excitation of the nervous system, leading to various effects depending on the specific type of GABA receptor they target.
GABA antagonists are used in medical treatments for certain conditions, such as sleep disorders, depression, and cognitive enhancement. However, they can also have adverse effects, including anxiety, agitation, seizures, and even neurotoxicity at high doses. Examples of GABA antagonists include picrotoxin, bicuculline, and flumazenil.
Baclofen is a muscle relaxant and antispastic medication. It is primarily used to treat spasticity, a common symptom in individuals with spinal cord injuries, multiple sclerosis, cerebral palsy, and other neurological disorders that can cause stiff and rigid muscles.
Baclofen works by reducing the activity of overactive nerves in the spinal cord that are responsible for muscle contractions. It binds to GABA-B receptors in the brain and spinal cord, increasing the inhibitory effects of gamma-aminobutyric acid (GABA), a neurotransmitter that helps regulate communication between nerve cells. This results in decreased muscle spasticity and improved range of motion.
The medication is available as an oral tablet or an injectable solution for intrathecal administration, which involves direct delivery to the spinal cord via a surgically implanted pump. The oral formulation is generally preferred as a first-line treatment due to its non-invasive nature and lower risk of side effects compared to intrathecal administration.
Common side effects of baclofen include drowsiness, weakness, dizziness, headache, and nausea. Intrathecal baclofen may cause more severe side effects, such as seizures, respiratory depression, and allergic reactions. Abrupt discontinuation of the medication can lead to withdrawal symptoms, including hallucinations, confusion, and increased muscle spasticity.
It is essential to consult a healthcare professional for personalized medical advice regarding the use and potential side effects of baclofen.
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.
GABA (gamma-aminobutyric acid) receptors are a type of neurotransmitter receptor found in the central nervous system. They are responsible for mediating the inhibitory effects of the neurotransmitter GABA, which is the primary inhibitory neurotransmitter in the mammalian brain.
GABA receptors can be classified into two main types: GABA-A and GABA-B receptors. GABA-A receptors are ligand-gated ion channels, which means that when GABA binds to them, it opens a channel that allows chloride ions to flow into the neuron, resulting in hyperpolarization of the membrane and decreased excitability. GABA-B receptors, on the other hand, are G protein-coupled receptors that activate inhibitory G proteins, which in turn reduce the activity of calcium channels and increase the activity of potassium channels, leading to hyperpolarization of the membrane and decreased excitability.
GABA receptors play a crucial role in regulating neuronal excitability and are involved in various physiological processes such as sleep, anxiety, muscle relaxation, and seizure control. Dysfunction of GABA receptors has been implicated in several neurological and psychiatric disorders, including epilepsy, anxiety disorders, and insomnia.
The cerebellar nuclei are clusters of neurons located within the white matter of the cerebellum, a region of the brain responsible for motor coordination, balance, and fine movement regulation. There are four main pairs of cerebellar nuclei: the fastigial, interpositus, dentate, and vestibular nuclei. These nuclei receive input from various parts of the cerebellar cortex and project to different areas of the brainstem and thalamus, contributing to the regulation of muscle tone, posture, and movement.
Flunitrazepam is a benzodiazepine drug, which has sedative, hypnotic, muscle relaxant, and anticonvulsant properties. Its primary use is for the treatment of severe insomnia and occasionally for managing anxiety disorders. It works by enhancing the effects of gamma-aminobutyric acid (GABA), a neurotransmitter in the brain that inhibits the activity of nerve cells and produces a calming effect.
Flunitrazepam is also known by its brand name, Rohypnol, and has gained notoriety for its use as a date-rape drug due to its ability to cause sedation, amnesia, and muscle relaxation at high doses. It is important to note that flunitrazepam is a controlled substance in many countries and its use without a prescription is illegal.
Picrotoxin is a toxic, white, crystalline compound that is derived from the seeds of the Asian plant Anamirta cocculus (also known as Colchicum luteum or C. autummale). It is composed of two stereoisomers, picrotin and strychnine, in a 1:2 ratio.
Medically, picrotoxin has been used as an antidote for barbiturate overdose and as a stimulant to the respiratory center in cases of respiratory depression caused by various drugs or conditions. However, its use is limited due to its narrow therapeutic index and potential for causing seizures and other adverse effects.
Picrotoxin works as a non-competitive antagonist at GABA (gamma-aminobutyric acid) receptors in the central nervous system, blocking the inhibitory effects of GABA and increasing neuronal excitability. This property also makes it a convulsant agent and explains its use as a research tool to study seizure mechanisms and as an insecticide.
It is important to note that picrotoxin should only be used under medical supervision, and its handling requires appropriate precautions due to its high toxicity.
GABA-A receptor antagonists are pharmacological agents that block the action of gamma-aminobutyric acid (GABA) at GABA-A receptors. GABA is the primary inhibitory neurotransmitter in the central nervous system, and it exerts its effects by binding to GABA-A receptors, which are ligand-gated chloride channels. When GABA binds to these receptors, it opens the chloride channel, leading to an influx of chloride ions into the neuron and hyperpolarization of the membrane, making it less likely to fire.
GABA-A receptor antagonists work by binding to the GABA-A receptor and preventing GABA from binding, thereby blocking the inhibitory effects of GABA. This can lead to increased neuronal excitability and can result in a variety of effects depending on the specific antagonist and the location of the receptors involved.
GABA-A receptor antagonists have been used in research to study the role of GABA in various physiological processes, and some have been investigated as potential therapeutic agents for conditions such as anxiety, depression, and insomnia. However, their use is limited by their potential to cause seizures and other adverse effects due to excessive neuronal excitation. Examples of GABA-A receptor antagonists include picrotoxin, bicuculline, and flumazenil.
GABA-B receptors are a type of G protein-coupled receptor that is activated by the neurotransmitter gamma-aminobutyric acid (GABA). These receptors are found throughout the central nervous system and play a role in regulating neuronal excitability. When GABA binds to GABA-B receptors, it causes a decrease in the release of excitatory neurotransmitters and an increase in the release of inhibitory neurotransmitters, which results in a overall inhibitory effect on neuronal activity. GABA-B receptors are involved in a variety of physiological processes, including the regulation of muscle tone, cardiovascular function, and pain perception. They have also been implicated in the pathophysiology of several neurological and psychiatric disorders, such as epilepsy, anxiety, and addiction.
Nipecotic acids are a class of compounds that function as GABA transaminase inhibitors. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the central nervous system, and its levels are regulated by enzymes such as GABA transaminase.
Nipecotic acids work by inhibiting this enzyme, leading to an increase in GABA levels in the brain. This can have various effects on the nervous system, including sedative, hypnotic, and anticonvulsant actions. Some nipecotic acid derivatives are used in research as tools for studying the role of GABA in the brain, while others have been investigated for their potential therapeutic uses in treating conditions such as anxiety, insomnia, and epilepsy.
It's important to note that nipecotic acids and their derivatives can have significant side effects and toxicity, and they are not approved for use as medications in most countries. Therefore, they should only be used under the close supervision of a trained medical professional for research purposes.
I'm sorry for any confusion, but "Oxazoles" is not a medical term, it is a chemical term. Oxazoles are heterocyclic aromatic organic compounds that contain a five-membered ring made up of one nitrogen atom, one oxygen atom, and three carbon atoms. They have the molecular formula C4H4NO.
Oxazoles do not have specific medical relevance, but they can be found in some natural and synthetic substances, including certain drugs and bioactive molecules. Some oxazole-containing compounds have been studied for their potential medicinal properties, such as anti-inflammatory, antimicrobial, and anticancer activities. However, these studies are primarily within the field of chemistry and pharmacology, not medicine itself.
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.
GABA (gamma-aminobutyric acid) agents are pharmaceutical drugs that act as agonists at the GABA receptors in the brain. GABA is the primary inhibitory neurotransmitter in the central nervous system, and it plays a crucial role in regulating neuronal excitability.
GABA agents can enhance the activity of GABA by increasing the frequency or duration of GABA-mediated chloride currents at the GABA receptors. These drugs are often used as anticonvulsants, anxiolytics, muscle relaxants, and sedatives due to their ability to reduce neuronal excitability and promote relaxation.
Examples of GABA agents include benzodiazepines, barbiturates, non-benzodiazepine hypnotics, and certain anticonvulsant drugs such as gabapentin and pregabalin. It is important to note that while these drugs can be effective in treating various medical conditions, they also carry the risk of dependence, tolerance, and adverse effects, particularly when used at high doses or for prolonged periods.
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.
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.
GABA-B receptor agonists are substances that bind to and activate GABA-B receptors, which are G protein-coupled receptors found in the central nervous system. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the brain, and its activation leads to decreased neuronal excitability.
GABA-B receptor agonists can produce various effects on the body, including sedation, anxiolysis, analgesia, and anticonvulsant activity. Some examples of GABA-B receptor agonists include baclofen, gabapentin, and pregabalin. These drugs are used in the treatment of a variety of medical conditions, such as muscle spasticity, epilepsy, and neuropathic pain.
It's important to note that while GABA-B receptor agonists can have therapeutic effects, they can also produce side effects such as dizziness, weakness, and respiratory depression, especially at high doses or in overdose situations. Therefore, these drugs should be used with caution and under the supervision of a healthcare provider.
"Long-Evans" is a strain of laboratory rats commonly used in scientific research. They are named after their developers, the scientists Long and Evans. This strain is albino, with a brownish-black hood over their eyes and ears, and they have an agouti (salt-and-pepper) color on their backs. They are often used as a model organism due to their size, ease of handling, and genetic similarity to humans. However, I couldn't find any specific medical definition related to "Long-Evans rats" as they are not a medical condition or disease.
Secobarbital is a barbiturate medication that is primarily used for the treatment of short-term insomnia and as a preoperative sedative. It works by depressing the central nervous system, producing a calming effect and helping to induce sleep. Secobarbital has a rapid onset of action and a relatively short duration of effect.
It is available in various forms, including capsules and injectable solutions, and is typically prescribed for use on an as-needed basis rather than as a regular medication. Secobarbital can be habit-forming and carries a risk of dependence and withdrawal, so it should only be used under the close supervision of a healthcare provider.
It's important to note that Secobarbital is not commonly prescribed in modern medical practice due to its high potential for abuse and the availability of safer and more effective sleep aids.
Pentobarbital is a barbiturate medication that is primarily used for its sedative and hypnotic effects in the treatment of insomnia, seizure disorders, and occasionally to treat severe agitation or delirium. It works by decreasing the activity of nerves in the brain, which produces a calming effect.
In addition to its medical uses, pentobarbital has been used for non-therapeutic purposes such as euthanasia and capital punishment due to its ability to cause respiratory depression and death when given in high doses. It is important to note that the use of pentobarbital for these purposes is highly regulated and restricted to licensed medical professionals in specific circumstances.
Like all barbiturates, pentobarbital has a high potential for abuse and addiction, and its use should be closely monitored by a healthcare provider. It can also cause serious side effects such as respiratory depression, decreased heart rate, and low blood pressure, especially when used in large doses or combined with other central nervous system depressants.
Isoxazoles are not a medical term, but a chemical compound. They are organic compounds containing a five-membered ring consisting of one nitrogen atom, one oxygen atom, and three carbon atoms. Isoxazoles have various applications in the pharmaceutical industry as they can be used to synthesize different drugs. Some isoxazole derivatives have been studied for their potential medicinal properties, such as anti-inflammatory, analgesic, and antipyretic effects. However, isoxazoles themselves are not a medical diagnosis or treatment.
Diazepam is a medication from the benzodiazepine class, which typically has calming, sedative, muscle relaxant, and anticonvulsant properties. Its medical uses include the treatment of anxiety disorders, alcohol withdrawal syndrome, end-of-life sedation, seizures, muscle spasms, and as a premedication for medical procedures. Diazepam is available in various forms, such as tablets, oral solution, rectal gel, and injectable solutions. It works by enhancing the effects of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain, which results in the modulation of nerve impulses in the brain, producing a sedative effect.
It is important to note that diazepam can be habit-forming and has several potential side effects, including drowsiness, dizziness, weakness, and impaired coordination. It should only be used under the supervision of a healthcare professional and according to the prescribed dosage to minimize the risk of adverse effects and dependence.
Chlormethiazole is a sedative and anticonvulsant drug, which is primarily used in the treatment of symptoms associated with alcohol withdrawal, such as agitation, tremors, and seizures. It belongs to the class of drugs known as thiazoles and exerts its therapeutic effects by acting on the central nervous system (CNS).
The chemical formula for Chlormethiazole is C4H5ClN2S. It has a white to off-white crystalline appearance and is soluble in water, alcohol, and chloroform. In addition to its use as a sedative and anticonvulsant, Chlormethiazole has also been used in the treatment of anxiety, insomnia, and various other neurological disorders.
It's important to note that Chlormethiazole can be habit-forming and should only be used under the close supervision of a healthcare professional. Additionally, it may interact with other medications and medical conditions, so it's essential to discuss any potential risks and benefits with a doctor before using this medication.
Muscimol
Oneirogen
Antiemetic
Ibotenic acid
Mushroom poisoning
Amanita muscaria var. guessowii
Amanita
Isoguvacine
R. Marthanda Varma
Rostral ventromedial medulla
Erminio Costa
Muscazone
Thiomuscimol
Legal status of psychoactive Amanita mushrooms
Allopregnanolone
Amanita ibotengutake
GABAA receptor
Amanita crenulata
Amanita chrysoblema
NMDA receptor antagonist
Amanita persicina
Psychoactive drug
Recreational drug use
Isoxazole
Between-systems memory interference model
Amanita gemmata
GABAA receptor positive allosteric modulator
CL-218,872
Quisqualamine
Dorsomedial hypothalamic nucleus
Muscimol - Wikipedia
Muscimol - Posts - Trusted Mushrooms
Buy Muscimol Gummies | Shop Muscimol Gummies
Muscimol: Exploring Its Effects, Uses, and Potential Benefits
Mushroom Toxicity: Practice Essentials, Pathophysiology, Etiology
Muscimol, GABA Agonists, and GABA - Amanita Research Forum
Causal role for the primate superior colliculus in the computation of evidence for perceptual decisions | Nature Neuroscience
Lateral geniculate neurons projecting to primary visual cortex show ocular dominance plasticity in adult mice | Nature...
Fluidization of brain membranes by A2C does not produce anesthesia and does not augment muscimol-stimulated 36Cl- influx.
Mushroom Poisoning Syndromes - North American Mycological Association
Revisiting the Role of Infralimbic Cortex in Fear Extinction with Optogenetics | Journal of Neuroscience
Can Psychedelic Therapies open a New Frontier in Mental Healthcare (Or Will the Bubble Burst?) | Frontiers Research Topic
Erowid Psychoactive Amanitas Vault : Dosage
Guide to Confirming an Etiology in Foodborne Disease Outbreak | Foodborne Outbreaks | Food Safety | CDC
Distribution of GABA(C)-like responses among acutely dissociated rat retinal neurons
Uusi-Oukari M[au] - Search Results - PubMed
Specific Involvement of Human Parietal Systems and the Amygdala in the Perception of Biological Motion | Journal of Neuroscience
Amanita muscaria, the fly agaric, Tom Volk's Fungus of the Month for December1999
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Erowid.org: Erowid Reference 7227 : The ontogeny of GABAergic enhancement of the gamma-hydroxybutyrate model of generalized...
Ibotenic acid (CAS 2552-55-8): R&D Systems
Convection-enhanced delivery of M13 bacteriophage to the brain in: Journal of Neurosurgery Volume 117 Issue 2 (2012) Journals
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PDF) The role of retinal photoreceptors in the regulation of circadian rhythms
Fazan G invoice cb - DemotiX
A Single Glycine Residue at the Entrance to the First Membrane-Spanning Domain of the γ-Aminobutyric Acid Type A Receptor β2...
The Atlantean Conspiracy: Santa Claus the Magic Mushroom
Ibotenic acid and muscimol6
- Amanita muscaria contains two primary active compounds, ibotenic acid and muscimol. (vidacap.com)
- All of the mushrooms that contain ibotenic acid and muscimol also sometimes contain muscarine (a toxin that got the name muscarine because it was first isolated from Amanita muscaria in the late 1800s). (namyco.org)
- Thus, patients sometimes also suffer muscarinic symptoms as well as symptoms of ibotenic acid and muscimol poisoning. (namyco.org)
- Most fruiting bodies contain two toxins, ibotenic acid and muscimol. (wisc.edu)
- Central actions of ibotenic acid and muscimol. (rndsystems.com)
- The toxins ibotenic acid and muscimol are not lethal to humans but in rare instances can cause death in dogs. (namyco.org)
Receptors11
- Muscimol is a potent and selective orthosteric agonist for the GABAA receptors and displays sedative-hypnotic, depressant and hallucinogenic psychoactivity. (wikipedia.org)
- GABAA receptors are widely distributed in the brain, and so when muscimol is administered, it alters neuronal activity in multiple regions including the cerebral cortex, hippocampus, and cerebellum. (wikipedia.org)
- While muscimol is normally thought of as a selective GABAA agonist with exceptionally high affinity to GABAA-delta receptors, it is also a partial agonist at the GABAA-rho receptor, and so its range of effects results from a combined action on more than one GABAA receptor subtype. (wikipedia.org)
- Therefore, muscimol can bind with GABA receptors, specifically GABA-A, and mimic the neurotransmitter's effects. (vidacap.com)
- Extrasynaptic δ-GABA A receptors are high-affinity muscimol receptors. (nih.gov)
- Using the baculovirus expression system in Spodoptera frugiperda 9 cells, anesthetic-induced enhancement of [ 3 H]muscimol and [ 3 H]flunitrazepam binding in receptors containing the β 2 (G219F) point mutation displayed a significantly reduced efficacy in modulation by all four i.v. anesthetics tested. (aspetjournals.org)
- Conversely, the homologous point mutation in ρ 1 receptors (F261G) changed the i.v. anesthetic-insensitive receptor to confer anesthetic modulation of [ 3 H]muscimol binding. (aspetjournals.org)
- Although ligand binding displayed comparable K D values for muscimol among wild-type, α 1 β 2 γ 2 , and mutant receptors, patch-clamp recordings showed that α 1 β 2 (G219F)γ 2 receptors had a significantly more potent response to GABA than did α 1 β 2 γ 2 or α 1 (G223F)β 2 γ 2 . (aspetjournals.org)
- The influence of γ-aminobutyric type-A (GABA A ) receptors agonist (muscimol hydrobromide, 0.1 µg/0.5 µl) injections into the right or left basolateral amygdala (BLA) on the behavior of high-an- xiety (HA) and low-anxiety (LA) rats subjected to the elevated plus-maze (EPM) test was investigated. (scirp.org)
- Muscimol is a potent agonist of GABA-A RECEPTORS and is used mainly as an experimental tool in animal and tissue studies. (bvsalud.org)
- Although muscimol is a well-characterized agonist for neuronal GABAA receptors, muscimol protection is not altered by GABAA receptor antagonists or recapitulated by other GABAA agonists, suggesting that muscimol acts via a novel mechanism. (bvsalud.org)
GABA12
- Muscimol is a potent GABAA agonist, activating the receptor for the brain's principal inhibitory neurotransmitter, GABA. (wikipedia.org)
- Muscimol binds to the same site on the GABAA receptor complex as GABA itself, as opposed to other GABAergic drugs such as barbiturates and benzodiazepines which bind to separate regulatory sites. (wikipedia.org)
- Because of its similarities to GABA, muscimol could help slow down signals in the central nervous system. (vidacap.com)
- Muscimol is a non-addictive GABA agonist. (amanitaresearch.com)
- This cannot be explained by eye-specific cortical changes propagating to dLGN via cortico-thalamic feedback because the shift in dLGN responses was largely resistant to cortical inactivation using the GABA A receptor agonist muscimol. (nature.com)
- In RCs, an asymmetric co-responsive pattern was observed between GABA- and muscimol-evoked events. (nih.gov)
- Muscimol-sensitive RCs responded well to GABA, but not all GABA-sensitive RCs responded to muscimol. (nih.gov)
- In GABA-sensitive BCs, muscimol responses were typically weak or absent. (nih.gov)
- The GHB seizure was quantitated in developing and adult rats in the presence of varying doses of the GABAa agonist muscimol or intracerebroventricularly (i.c.v.) administered GABA. (erowid.org)
- Both GABA and muscimol potentiated GHB-induced seizures in an age-dependent fashion. (erowid.org)
- The developmental sensitivity of the rat to GHB seizure correlated with enhancement of the seizure by muscimol and GABA, and both phenomena parallel the maturation of thalamocortical recruiting mechanisms thought to play a role in the pathogenesis of the bilaterally synchronous spike wave discharges that characterize generalized absence seizures. (erowid.org)
- Es un potente agonista de los receptores GABA-A y se utiliza principalmente como herramienta experimental en estudios sobre animales y tejidos. (bvsalud.org)
Amanita18
- Muscimol (also known as agarin or pantherine) is one of the principal psychoactive constituents of Amanita muscaria and related species of mushroom. (wikipedia.org)
- Muscimol is one of the psychoactive compounds responsible for the effects of Amanita muscaria intoxication. (wikipedia.org)
- Ibotenic acid, a neurotoxic secondary metabolite of Amanita muscaria, serves as a prodrug to muscimol when the mushroom is ingested or dried, converting to muscimol via decarboxylation. (wikipedia.org)
- Muscimol is produced in the mushrooms Amanita muscaria (fly agaric) and Amanita pantherina, along with muscarine (which is present in trace amounts and it is not active), muscazone, and ibotenic acid. (wikipedia.org)
- When consumed, a substantial percentage of muscimol goes un-metabolized and thus excreted in urine, a phenomenon exploited by practitioners of the traditional entheogenic use of Amanita muscaria. (wikipedia.org)
- Muscimol was first isolated from Amanita pantherina by Onda in 1964, and thought to be an amino acid or peptide. (wikipedia.org)
- Muscimol can be extracted from the flesh of the Amanita muscaria by treatment with boiling water, followed by rapid cooling, and further treatment with a basic resin. (wikipedia.org)
- In instances where pure muscimol is not required, such as recreational or spiritual use, a crude extract is often prepared by simmering dried Amanita muscaria in water for thirty minutes. (wikipedia.org)
- Muscimol is one of the key active compounds in Amanita muscaria mushrooms. (vidacap.com)
- Ibotenic acid is predominant in raw Amanita muscaria mushrooms, but preparing them in a specific way converts it into muscimol . (vidacap.com)
- Although muscimol is understudied, many people use Amanita muscaria extracts to alleviate common complaints. (vidacap.com)
- Another option is to choose lab-tested products like our amanita gummies , so you know exactly how much muscimol is in each serving. (vidacap.com)
- Amanita Mushroom Gummies are small gummy cubes infused with Amanita muscaria mushroom extract and muscimol, the main mind-expanding compound in the mushroom. (exhalewell.com)
- Our experts carefully dry the Amanita at the ideal temperature, which helps to eliminate ibotenic acid and preserve muscimol. (exhalewell.com)
- To make our Amanita Mushroom Gummies, we take muscimol extract from these dried caps and infuse it into a base of MCT oil and pectin. (exhalewell.com)
- Muscimol is one of the most well-known compounds found in Amanita muscaria mushrooms. (fsinutrition.com)
- Thanks to the presence of compounds like muscimol and ibotenic acid, Amanita muscaria mushroom gummies have the potential to support cognitive function. (fsinutrition.com)
- Muscimol, found in Amanita muscaria mushrooms, has calming properties that can help reduce anxiety and promote relaxation. (fsinutrition.com)
Compounds3
- However, the precise ratios of compounds will depend upon the preparation method , with partial or complete decarboxylation resulting in a higher muscimol content and lower levels of ibotenic acid. (vidacap.com)
- The mushroom's psychoactive compounds, including muscimol and ibotenic acid, are responsible for its hallucinogenic effects. (wlnaturalhealth.com)
- These compounds include ibotenic acid (which is mildly toxic) and muscimol (which is responsible for most of the effects). (aheartisaspade.com)
Gummies2
- Explore our enticing selection of Muscimol Gummies , encompassing an array of flavors tailored to your desires, including strawberry, grape, blue raspberry, and more. (mn-nice-ethnobotanicals.com)
- Our plant-based gummies are also lab-tested to confirm they contain an equal and consistent amount of muscimol. (exhalewell.com)
Mushrooms1
- Moreover, mushrooms naturally differ in their concentration of active chemicals, and humans naturally differ in their responses to muscimol. (vidacap.com)
Psychoactive4
- In A. muscaria, the layer just below the skin of the cap contains the highest amount of muscimol, and is therefore the most psychoactive portion. (wikipedia.org)
- Muscimol is probably best known as a psychoactive compound, but it could have some medicinal properties, too. (vidacap.com)
- Estimates vary regarding how much muscimol constitutes a dose, with 6-10mg being suggested as the threshold for psychoactive effects. (vidacap.com)
- Their main psychoactive ingredient is 'muscimol,' as well as trace amounts of DMT, an entheogen naturally produced in the brain's pineal gland. (atlanteanconspiracy.com)
Receptor1
- To clarify what they're saying is that the Muscimol works on a different part of the receptor that does not cause tolerance or down-regulation like benzos? (amanitaresearch.com)
Ingestion1
- After ingestion, a small amount of ibotenic acid decarboxylates into muscimol, which produces the intoxication. (erowid.org)
Potent1
- The adult dose of 1 mg/kg muscimol was extremely potent in rats less than 28 days of age and resulted in the death of all younger animals tested secondary to profound hypothermia. (erowid.org)
Zolpidem2
- The hallucinogenic effect produced by muscimol is most closely comparable to the hallucinogenic/Lilliputian side effects produced by some other GABAergic drugs such as zolpidem. (wikipedia.org)
- Effects of buspirone, diazepam, and zolpidem on open field behavior, and brain [3H]muscimol binding after buspirone pretreatment. (bvsalud.org)
Inactivation1
- Studies in rats have shown that the inactivation of this area of the brain through the use of muscimol and ibotenate will inhibit fear learning and the startle reflex. (wisc.edu)
Isoxazole2
- Muscimol is a semi-rigid isoxazole containing both alcohol and aminomethyl substituents. (wikipedia.org)
- The entheogenic constituents of A. muscaria are ibotenic acid (alpha-amino3-hydroxy-5-isoxazole acetic acid), muscimol (3hydroxy-5-aminomethy1 isoxazole), and possibly muscazone ( Ott ). (erowid.org)
Rats2
- A dose of 0.1 mg/kg muscimol was associated with a significant prolongation of GHB seizure in rats less than 35 days of age, but had no effect on older animals. (erowid.org)
- No effect was observed upon administration of muscimol to LA rats. (scirp.org)
Doses1
- In patients with Huntington's disease and chronic schizophrenia, oral doses of muscimol have been found to cause a rise of both prolactin and growth hormone. (wikipedia.org)
Relaxation1
- Although there is little clinical research into the effects of muscimol, anecdotal reports suggest it induces a state of relaxation, followed by drowsiness and deep sleep. (vidacap.com)
Trace amounts1
- This test verifies the amount of muscimol and checks for any trace amounts of ibotenic acid. (exhalewell.com)
Hallucinogenic1
- Atypical of the effect profile of sedative drugs generally however, muscimol, like Z-drugs, can cause hallucinogenic changes in perception. (wikipedia.org)
Compound2
- However, little is known about whether muscimol is the compound responsible for these effects, the optimal dosage, and the safety of long-term use. (vidacap.com)
- In light of this, we describe an HPLC HILIC analytical method for the evaluation of the content of the anticancer compound ergosterol (ERG) and the neuroactive alkaloids ibotenic acid (IBO) and muscimol (MUS) that contribute significantly to the unpleasant physiological syndrome associated with A. muscaria consumption. (bvsalud.org)
Reduces1
- In addition, we demonstrate that muscimol reduces lethality during LPS-induced septic shock. (bvsalud.org)
Clinical1
- Muscimol went under clinical trial phase I for epilepsy, but the trial was discontinued. (wikipedia.org)
Commonly2
- Muscimol is commonly portrayed as a tautomer, where it adopts an amide-like configuration. (wikipedia.org)
- One commonly asked question is: "Is muscimol safe? (vidacap.com)
Brain2
Consumption1
- The effects of muscimol begin around one hour after consumption, peaking at 3 hours, and lasting a total of 10-24 hours. (wikipedia.org)
Effects1
- Anxiolytic-like effects (increase of open-arm entries and open-arm time) was revealed only after administration of muscimol into the left (but not right) amygdala of HA animals. (scirp.org)
Activity2
- Taken orally, muscimol displays activity at 10-15 mg. (erowid.org)
- Here, we show that muscimol has reversible activity to prevent cellular lysis without affecting earlier pyroptotic events. (bvsalud.org)
Results1
- A subsequent elution with ammonium hydroxide and recrystallization from alcohol results in pure muscimol. (wikipedia.org)
Regions1
- In both regions, muscimol interfered with preference for the stressed juvenile and naive adult, indicating that these regions are necessary for appropriate social affective behavior. (bvsalud.org)
Small1
- We previously identified muscimol as a small molecule that prevents plasma membrane rupture during pyroptosis via an unidentified mechanism. (bvsalud.org)
Local1
- In separate experiments, the BLA or the insula were inhibited by local infusion of muscimol (100ng/side in 0.5µL saline) or vehicle prior to SAP tests. (bvsalud.org)
Primary1
- Muscimol appears to be the primary intoxicant. (erowid.org)
Test1
- During a test involving rabbits connected to an EEG, muscimol presented with a distinctly synchronized EEG tracing. (wikipedia.org)