• 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)
  • While these traditional AEDs have had a profound effect by reducing the expression of epileptic seizures, their function invariably elicits some impairment of the normal neuronal excitability underlying cognitive function [6-8]. (jle.com)
  • Once seizures occur, the epileptic disease state probably continues to progress, with each seizure having the potential to induce additional neuronal alterations that may further lower seizure thresholds [19]. (jle.com)
  • While anticonvulsants reduce the duration or frequency of seizures by suppressing neuronal excitation or excitability, real antiepileptogenic agents would act by blocking the initial epileptogenic process or by altering the epileptic disease state after the seizure onset [11]. (jle.com)
  • Ramifications of progesterone against kainic acid-induced seizures may also be sex-specific: in females, progesterone provides anticonvulsant results while in men the effect is certainly proconvulsant (Nicoletti et al. (nos-nop.org)
  • Ramifications of feminine sex human hormones on seizures and neuronal excitability in females The need for sex hormone actions in the mind is certainly underscored by reviews displaying that neurons and glia are outfitted for local creation of steroid human hormones in the central anxious program (CNS) (Lavaque et al. (nos-nop.org)
  • Scholars@Duke publication: Seizures, cell death, and mossy fiber sprouting in kainic acid-treated organotypic hippocampal cultures. (duke.edu)
  • We report here that that application of the convulsant, kainic acid, to organotypic hippocampal explant cultures induces seizures, neuronal cell death, and subsequent dramatic mossy fiber sprouting with a similar laminar preference and time-course to that seen in intact animals. (duke.edu)
  • Indeed, functional studies in animals, mainly using antisense oligonucleotides (ASOs) termed antagomirs, have demonstrated that targeting miRNAs can alter evoked and spontaneous seizures and neuropathological outcomes including neuronal loss and gliosis [ 11 ]. (researchsquare.com)
  • We investigated the two exclusively ketogenic amino acids, L-leucine and L-lysine, and found that only L-leucine potently protects mice when administered prior to the onset of seizures induced by kainic acid injection, but not by inducing ketosis. (johnshopkins.edu)
  • Compared with WT mice, TNF-α KO mice were more susceptibile to KA-induced neurotoxicity, as demonstrated by more severe seizures, measurable behavior changes, greater neuronal degeneration in hippocampus, elevated glial activation and NO production. (uaeu.ac.ae)
  • Journal Article] Limb-clasping, cognitive deficit and increased vulnerability to kainic acid - induced seizures in neuronal GPI anchor deficiency mouse models. (nii.ac.jp)
  • 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)
  • Differential 24 h responsiveness of Prox1-expressing precursor cells in adult hippocampal neurogenesis to physical activity, environmental enrichment, and kainic acid-induced seizures. (mdc-berlin.de)
  • Also, infusion with kainic acid in the hippocampus of animals results in major damage of pyramidal neurons and subsequent seizure activity. (wikipedia.org)
  • Domoic acid has been associated with necrosis of the glutamate-rich hippocampus and amygdala in autopsied cases. (medscape.com)
  • Alternatively, in feminine hippocampus, estradiol didn't enhance neuronal excitability. (nos-nop.org)
  • 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)
  • This study investigated calcium/calmodulin kinase II (CaMKII) activity related to long-standing neuronal injury of the hippocampus in kainate (KA)-induced experimental temporal lobe epilepsy. (koreamed.org)
  • Le Gal La Salle G, Rougon G, Valin A. The embryonic type of neural cell floor molecule (E-NCAM) within the rat hippocampus and its reexpression on glial cells following kainic acid-induced status epilepticus. (chloeliemofficial.com)
  • More recently we have demonstrated that C/EBPβ regulates the expression of several genes involved in inflammatory processes and brain injury [ 14 ] and mice lacking C/EBPβ showed a reduced inflammatory response after kainic acid injection and exhibited a dramatic reduction in pyramidal cell loss in the CA1 and CA3 subfields of the hippocampus [ 15 ]. (biomedcentral.com)
  • 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 pathophysiological relevance of this observation was investigated in synaptosomes and post-synaptic densities isolated from rat hippocampi and cerebral cortices following kainic acid-induced status epilepticus. (uandes.cl)
  • Here we reveal that TrkB-mediated activation of Akt protects against hippocampal neuronal death in vivo following status epilepticus. (jneurosci.org)
  • These findings strengthen the evidence that desirable and undesirable consequences of status epilepticus-induced TrkB activation are mediated by distinct signaling pathways downstream of this receptor. (jneurosci.org)
  • neuroscience research neurodegenerative agent modeling of epilepsy modeling of Alzheimer's disease Dihydrokainic acid Domoic acid Kainate receptor Carlson NR (2013). (wikipedia.org)
  • Since the development of epilepsy is a multistep progressive process [12], there may be several mechanisms in addition to the neuronal excitability and hypersynchronization associated with the paroxysmal event that are susceptible to pharmacologic intervention. (jle.com)
  • On the contrary, knockdown of Sprouty proteins increases proliferation of activated astrocytes and, consequently, reduces secondary brain damage in neuronal lesion models such as kainic acid-induced epilepsy or endothelin-induced ischemia. (springer.com)
  • Epilepsy is caused by abnormal coordinated firing of neuronal cells mainly due to disparity among excitatory and inhibitory neurotransmission [ 4 ] . (encyclopedia.pub)
  • Sequencing as well as functional studies using antisense oligonucleotides, indicate important roles for microRNAs during the development of epilepsy through targeting transcripts involved in neuronal structure, gliosis and inflammation. (researchsquare.com)
  • The P2X7 receptor was identified as a miR-22 target and co-injection of a P2X7 receptor antagonist mitigated the epilepsy phenotype in mice given the ASO inhibitor of miR-22 [ 16 ]. (researchsquare.com)
  • Since epilepsy is also supposed to constitute a comorbidity of DMD, it is hypothesized that dystrophin plays a role in neuronal excitability. (frontiersin.org)
  • Although activation of TrkB signaling promotes development of epilepsy in this context, it also reduces SE-induced neuronal death. (jneurosci.org)
  • The neuronal ceroid lipofuscinoses (NCLs) comprise a group of human neurodegenerative disorders (CLN1-CLN8) characterized by epilepsy, visual failure, psychomotor deterioration and accumulation of autofluorescent lipopigment in many tissues, especially in neurons [ 1 ]. (biomedcentral.com)
  • Gluconic acid, a natural organic acid enriched in fruits and honey, and the glucose oxidase enzyme, is shown herein to potently inhibit neonatal epilepsy both in vitro and in vivo. (justia.com)
  • Sodium gluconate is shown to inhibit epileptiform burst activity in cell cultures and protect neurons from kainic acid-induced cell death. (justia.com)
  • Glutamate is produced by the cell's metabolic processes and there are four major classifications of glutamate receptors: NMDA receptors, AMPA receptors, kainate receptors, and the metabotropic glutamate receptors. (wikipedia.org)
  • Neurosteroids are recognized for their non-genomic acute results by direct modulation of NMDA GABAA and receptors receptors. (nos-nop.org)
  • Nitric oxide (NO) has been proposed to down-regulate NMDA receptors (NMDA-Rs) in a homeostatic manner. (uandes.cl)
  • 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)
  • NMDA and benzodiazepine receptors have synergistic and antagonistic effects on precursor cells in adult hippocampal neurogenesis. (mdc-berlin.de)
  • In contrast, COX-2 null (knockout) mice exhibit less neuronal death following ischemia or challenge with NMDA [7]. (healthandwellnesssource.org)
  • Metabolism of arachidonic acid through cyclooxygenase (COX) enzymes is known to be actively involved in the neuroinflammatory events leading to neuronal death after ischemia. (southampton.ac.uk)
  • In EAE, excitotoxicity and axonal damage appear to contribute to the pathology of the disease, since -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) antagonists of GluRs can ameliorate the neurological deficits associated with the progression of the disease [14]. (healthandwellnesssource.org)
  • The α-amino-3-hydroxy-5-methyl-4-isoxazolopropionic acid receptor ( AMPA receptor ) is an ionic glutamate (iGluR) transmembrane receptor. (immune-system-research.com)
  • Besides, AMPA receptors are responsible for most of the rapid excitatory transmission in the central nervous system. (immune-system-research.com)
  • Now, we will introduce a selective noncompetitive AMPA receptor antagonist, CP-465022 . (immune-system-research.com)
  • At first, CP-465022 is a potent, and selective noncompetitive AMPA receptor antagonist with anticonvulsant activity. (immune-system-research.com)
  • CP-465022 provides a new tool to investigate the role of AMPA receptors in physiological and pathophysiological processes. (immune-system-research.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)
  • Excitotoxicity, a critical process in neurodegeneration, induces oxidative stress and neuronal death through mechanisms largely unknown. (nature.com)
  • Since oxidative stress activates protein kinase D1 (PKD1) in tumor cells, we investigated the effect of excitotoxicity on neuronal PKD1 activity. (nature.com)
  • Our results indicate that PKD1 inactivation underlies excitotoxicity-induced neuronal death and suggest that PKD1 inactivation may be critical for the accumulation of oxidation-induced neuronal damage during aging and in neurodegenerative disorders. (nature.com)
  • Several mechanisms of neuronal cell death have been proposed for HD, including excitotoxicity, oxidative stress, impaired energy metabolism, and apoptosis. (medscape.com)
  • Excitotoxicity refers to the neurotoxic effect of excitatory amino acids in the presence of excessive activation of postsynaptic receptors. (medscape.com)
  • Treatment of OPCs with an EP1/EP3 agonist 17 phenyl-trinor PGE2 reversed protection from a COX-2 inhibitor while inhibition of EP3 receptor protected OPCs from excitotoxicity. (healthandwellnesssource.org)
  • SMAD9 Transgenic mice that over-express neuronal COX-2 are more susceptible to excitotoxicity [5] and age-associated neuronal loss [6]. (healthandwellnesssource.org)
  • Kainic acid is an agonist for kainate receptors, a type of ionotropic glutamate receptor. (wikipedia.org)
  • Kainate receptors likely control a sodium channel that produces excitatory postsynaptic potentials (EPSPs) when glutamate binds. (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)
  • In mice, amitriptyline was further shown to suppress neuronal apoptosis caused by the neuroexitotoxin, kainic acid, in a TrkA-dependent manner. (drugdiscoveryopinion.com)
  • Excitotoxic production of ROS elevates death-associated protein kinase (DAPK) activity, which provokes neuronal apoptosis in cerebral ischemia and seizure models 8 . (nature.com)
  • His primary scientific interests are in Biochemistry, Reactive oxygen species, Glutamate receptor, Apoptosis and Cyclosporin a. (research.com)
  • This has identified a number of classes of AEDs that primarily suppress neuronal excitability by blocking Na + channels or enhancing inhibitory GABAergic activity [4, 5]. (jle.com)
  • 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)
  • Frode Fonnum combines subjects such as Kainic acid and Neurotoxicity with his study of Endocrinology. (research.com)
  • Neuronal PKD1 inactivation by pharmacological inhibition or lentiviral silencing in vitro, or by genetic inactivation in neurons in vivo, strongly enhances excitotoxic neuronal death. (nature.com)
  • The EP3 receptor was identified as a candidate contributing to OPC excitotoxic death based on pharmacological evidence. (healthandwellnesssource.org)
  • 2, 3] and [4] following induction of glutamate-receptor-mediated excitotoxic death. (healthandwellnesssource.org)
  • Therefore, pharmacological and genetic evidence reveals that COX-2 expression and activity contributes to neuronal excitotoxic cell death. (healthandwellnesssource.org)
  • Using this analogy as a framework for the role of COX-2 in death of oligodendrocytes (OLs), we showed that COX-2 is induced in OLs and OPCs following glutamate receptor (GluR) activation and renders these cells more susceptible to excitotoxic death [8]. (healthandwellnesssource.org)
  • In this study, we examined whether prostanoids (PGs) such as PGE2 and their receptors contribute to excitotoxic death of OPCs. (healthandwellnesssource.org)
  • Chemical stimulation, while more complicated than electrical stimulation, has the distinct advantage of activating cell bodies, but not nearby axons, because only cell bodies and subsequent dendrites contain glutamate receptors. (wikipedia.org)
  • Among newer AEDs, felbamate, gabapentin, tiagabine and topiramate proved to be neuroprotective agents against seizure, or ischemia-generated neuronal death. (jpccr.eu)
  • The stimuli to induce adipocyte differentiation in hBM-MSCs increase the gene transcription of the $CB_1$ receptor, TRPV1 and $PPAR{\gamma}$ . (koreascience.kr)
  • Expression of Cln8 in the developing and mature brain suggests roles for Cln8 in maturation, differentiation and supporting the survival of different neuronal populations. (biomedcentral.com)
  • Synaptic network activity induces neuronal differentiation of adult hippocampal precursor cells through BDNF signaling. (mdc-berlin.de)
  • In this regard, we have demonstrated that C/EBPβ serves as a critical factor in neuronal differentiation [ 13 ]. (biomedcentral.com)
  • Endocannabinoids can affect multiple cellular targets, such as cannabinoid (CB) receptors, transient receptor potential cation channel, subfamily V, member 1 (TRPV1) and peroxisome proliferator-activated receptor ${\gamma}$ ( $PPAR{\gamma}$ ). (koreascience.kr)
  • Cannabinoid receptor CB1 mediates baseline and activity-induced survival of new neurons in adult hippocampal neurogenesis. (mdc-berlin.de)
  • 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)
  • 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)
  • 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)
  • The neuronal ceroid lipofuscinoses (NCLs) are a group of inherited neurodegenerative disorders characterized by accumulation of autofluorescent material in many tissues, especially in neurons. (biomedcentral.com)
  • Neurotrophins - a family of proteins essential for the development, survival and function of neurons - exert their actions through two classes of receptor, Trk tyrosine kinase receptors and p75NTR. (drugdiscoveryopinion.com)
  • SE-induced activation of the BDNF receptor tyrosine kinase, TrkB, is one signaling pathway by which SE induces TLE. (jneurosci.org)
  • BDNF signaling thru TrkB receptor tyrosine kinase is one molecular mechanism promoting TLE. (jneurosci.org)
  • Work by multiple investigators including ourselves implicates the receptor tyrosine kinase, TrkB, and its canonical ligand, BDNF, as one signaling pathway by which SE induces development of TLE ( McNamara and Scharfman, 2012 ). (jneurosci.org)
  • The most striking neuropathology in HD occurs within the neostriatum, in which gross atrophy of the caudate nucleus and putamen is accompanied by selective neuronal loss and astrogliosis. (medscape.com)
  • The selective neuronal dysfunction and subsequent loss of neurons in the striatum, cerebral cortex, and other parts of the brain can explain the clinical picture seen in cases of HD. (medscape.com)
  • Prolonged (48 h) but not transient (4 h) kainic acid treatment caused regionally selective neuronal cell death. (duke.edu)
  • Domoic acid (DA) is structurally similar to the excitatory neurotransmitter glutamate. (medscape.com)
  • In the meanwhile, microglia express the metabotropic P2Y6 receptors, the activation of which by uridine 5'-diphosphate (UDP) triggers microglial phagocytosis in a concentration-dependent fashion. (elsevierpure.com)
  • Sprouting of the mossy fiber axons of the dentate granule cells is a structural neuronal plasticity found in the mature brain of epileptic humans and experimental animals. (duke.edu)
  • A paper recently published by eLife on forebrain cortical synaptic plasticity reports that retinoic acid (RA) alters synaptopodin-dependent metaplasticity in mouse dentate granule cells (Lenz et al. (preprints.org)
  • Conclusion Therefore, inhibitors MifaMurtide of the EP3 receptor appear to enhance survival of OPCs following toxic challenge and may help facilitate remyelination. (healthandwellnesssource.org)
  • For example, this disclosure relates to compositions that include, for example, one or more agents that decrease the concentration of cyclooxygenase-2, decrease the concentration of transient receptor potential cation channel subfamily V member 1, and/or decrease calcitonin gene-related peptide concentration. (justia.com)
  • Diverse signal recognition receptors and signal transduction pathways were defined which regulate cellular functions, metabolism and development. (mdpi.com)
  • As an alternative approach, growth factor receptors or components of their signal transduction machinery may be targeted directly. (springer.com)
  • The effect of AEA on $PPAR{\gamma}$ in hBM-MSCs may prevail over that on the $CB_1$ receptor mediated signal transduction, giving rise to the AEA-induced promotion of adipogenesis. (koreascience.kr)
  • 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)
  • To confirm production of kainic acid through the identified cluster, Chekan et al expressed the genes in Escherichia coli and validated the enzymatic functions of each proposed gene. (wikipedia.org)
  • The main mechanism involved in early tolerance is adaptation of membrane receptors, whereas gene activation with subsequent de novo protein synthesis dominates delayed tolerance. (biomedcentral.com)
  • [ 7 ] More recent data from striatal neuronal cultures transfected with mutant huntingtin and transgenic mice carrying the spinocerebellar ataxia-1 (SCA-1) gene (another CAG repeat disorder) suggest that NIIs may not be necessary or sufficient to cause neuronal cell death, but translocation into the nucleus is sufficient to cause neuronal cell death. (medscape.com)
  • Gene expression programmes drive many of the changes underlying network reorganisation in epileptogenesis, including neurodegeneration, astrogliosis, microgliosis, aberrant neurogenesis and restructured local and distant neuronal contacts, among other changes [ 3-5 ]. (researchsquare.com)
  • Previous studies from our laboratory indicated that C/EBPβ is implicated in inflammatory process and brain injury, since mice lacking this gene were less susceptible to kainic acid-induced injury. (biomedcentral.com)
  • The extent of gross striatal pathology, neuronal loss, and gliosis provides a basis for grading the severity of HD pathology (grades 0-4). (medscape.com)
  • A potential antiseizure role of dietary protein or of individual amino acids in the ketogenic diet is understudied. (johnshopkins.edu)
  • For an in vitro model to be feasible, the circuitry and receptors involved in convulsant-induced mossy fiber sprouting would have to be localized near the granule cells, rather than being dependent on long-range brain interconnections. (duke.edu)
  • Okadaic acid binds to intestinal epithelial cells and increases their permeability. (medscape.com)
  • The cellular and molecular determinants required for kainic acid-induced cell death and subsequent mossy fiber reorganization thus appear to be intrinsic to the hippocampal slice preparation, and are preserved in culture. (duke.edu)
  • Regional and cellular dystrophin distribution was evaluated in both human and rat hippocampi and in rat cerebellar tissue by immunofluorescent colocalization with neuronal (NeuN and calbindin) and glial (GFAP) markers. (frontiersin.org)
  • Functionally, dystrophin expressed in the CNS plays an important role in the clustering of neurotransmitter receptors and water- and ion channels to the cellular membrane. (frontiersin.org)
  • [ 4 ] which allows sodium influx and a small amount of potassium efflux-neuronal depolarization results. (medscape.com)
  • 2 Therefore, applying rapid therapies for treating SE, enhances neuroprotection and suppresses the long-term sequels such as epileptogenesis, neuronal damage and cognitive deficits. (j-epilepsy.org)
  • 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)
  • After a penetrating lesion within the central nervous system, astrocytes enlarge, divide, and participate in creating an setting that adversely affects neuronal regeneration. (chloeliemofficial.com)
  • In recent years, the search for intracellular signaling integrator downstream of receptor tyrosine kinases provided valuable novel substrates. (springer.com)
  • Glial-neuronal interactions as studied by cerebral metabolism of [2-13C]acetate and [1-13C]glucose: an ex vivo 13C NMR spectroscopic study. (research.com)
  • However, over recent years, it became clear that RTKs cannot be sufficiently activated by growth factors or receptor agonists in the adult and aging brain to exert significant neuroprotective or neurorestorative effects. (springer.com)
  • and the effects of EP3 receptor agonists and antagonists on OPC viability were examined. (healthandwellnesssource.org)
  • Thus, the present study was carried out to examine these mechanisms in aged animals by administering a control, 2 % SB- or 2 % BB-supplemented diet to aged Fischer 344 rats for 8 weeks to ascertain their effectiveness in reversing age-related deficits in behavioural and neuronal function. (cambridge.org)
  • The various areas that Frode Fonnum examines in his Glutamate receptor study include Amino acid, Glutamine, Neurotransmitter, Neuroscience and Metabolism. (research.com)
  • Logan A, Frautschy SA, Gonzalez AM, Baird A. A time course for the focal elevation of synthesis of basic fibroblast growth factor and one of its high-affinity receptors following a localized cortical mind damage. (chloeliemofficial.com)
  • Cultures treated with kainic acid for a prolonged period displayed a time- and dose-dependent increase in supragranular Timm staining reflective of increased mossy fiber innervation to this area. (duke.edu)
  • Direct visualization of mossy fiber axons with neurobiotin-labeling revealed that mossy fibers in kainic acid-treated cultures exhibited a dramatic increase in supragranular axonal branch points and synaptic boutons. (duke.edu)
  • channels both in neuronal cultures and in hippocampal slices. (justia.com)
  • Since ictogenesis and cognition are both mediated by neuronal excitability, it may not be possible to discover optimal non-impairing AEDs using traditional screens. (jle.com)
  • Thus, by applying genetically modified or kindled animals [9] it may be possible to discover new AEDs that inhibit the neuronal hypersynchronization leading to an ictal event, without interfering with normal neuronal excitability [10]. (jle.com)
  • Neurosteroids are accountable Lep mainly for great tuning of neuronal excitability by performing at synaptic and extrasynaptic receptors (Lambert et al. (nos-nop.org)
  • His study in Reactive oxygen species is interdisciplinary in nature, drawing from both Phospholipase A2, Medicinal chemistry, Nitric oxide and Phospholipase C. His study with Glutamate receptor involves better knowledge in Receptor. (research.com)
  • 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)
  • His Glutamate receptor research includes themes of Amino acid, Glutamic acid, Neurotransmitter, Biophysics and Dopamine. (research.com)
  • His Glutamic acid study combines topics in areas such as Free nerve ending, Calcium metabolism, Mammalian brain, Receptor and Aspartate binding. (research.com)
  • When neighboring cells are injured, the cells release or leak ATP into extracellular space and microglia rapidly move toward or extend a process to the nucleotides as chemotaxis through P2Y12 receptors. (elsevierpure.com)
  • Systemic administration of kainic acid in rats resulted in neuronal cell death in the hippocampal CA1 and CA3 regions, where increases in mRNA for P2Y6 receptors in activated microglia. (elsevierpure.com)
  • In this review, we summarize the role of Sprouties in the lesioned central and peripheral nervous system with particular reference to Sprouty2 that is upregulated in various experimental models of neuronal degeneration and regeneration. (springer.com)
  • Five days following KA treatment, immunohistochemical methods were used to assess neuronal degeneration and glial activation. (uaeu.ac.ae)
  • EPO activates the neuronal EPO receptor and, subsequently, JAK-2 and thereby PI3K. (jneurosci.org)
  • Oppositional effects of serotonin receptors 5-HT1a, 2, and 2c in the regulation of adult hippocampal neurogenesis. (mdc-berlin.de)
  • Intermediate progenitors in adult hippocampal neurogenesis: Tbr2 expression and coordinate regulation of neuronal output. (mdc-berlin.de)
  • This has led to a search for stable small molecules with neurotrophic activity and specificity for TrkA or TrkB receptors although, so far, none of the mimetics can fully reproduce the effects of NGF in animals. (drugdiscoveryopinion.com)
  • Writing in the journal Chemistry & Biology , researchers at Emory University School of Medicine have now shown that the tricyclic antidepressant, amitriptyline, which had been thought to act predominantly by blocking serotonin and noradrenaline transporters, interacts directly with the extracellular domain of both TrkA and TrkB receptors. (drugdiscoveryopinion.com)
  • Amitriptyline induced TrkA and TrkB homo- and heterodimerization and activation in mouse brain, but heterodimerization was found not to be required for Trk receptor activation. (drugdiscoveryopinion.com)
  • Truncation of the amitriptyline binding motif on TrkA, but not the corresponding region on TrkB, abolished the receptor homo- and heterodimerization. (drugdiscoveryopinion.com)
  • Importantly, genetic disruption of TrkB-Shc signaling exacerbated hippocampal neuronal death induced by SE. (jneurosci.org)
  • The reasons for this may involve receptor downregulation and truncation, among others [ 10 ]. (springer.com)
  • Domoic acid is produced by the diatom Nitzschia pungens . (medscape.com)
  • Therefore, chemical stimulation by kainic acid is more localized than electrical stimulation. (wikipedia.org)
  • Sortilin-related receptor with A-type repeats (SORLA) affects the amyloid precursor protein-dependent stimulation of ERK signaling and adult neurogenesis. (mdc-berlin.de)
  • We investigated spatial and temporal expression of Cln8 messenger ribonucleic acid (mRNA) using in situ hybridization, reverse transcriptase polymerase chain reaction (RT-PCR) and northern blotting. (biomedcentral.com)