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N-methyl-d-aspartate and nonn-methyl-d-aspartate receptors mediate seizures and CA1 hippocampal damage induced by dendrotoxin-K in rats

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TLDR
The present data on dendrotoxin K, together with the previously described pattern of neurotoxicity for alpha-dend rotoxin, show that these homologues act via different mechanisms and can be used effectively as complementary tools to study seizures and neuronal cell death.
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This article is published in Neuroscience.The article was published on 1996-04-01. It has received 24 citations till now.

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Altered glutamatergic transmission in neurological disorders: From high extracellular glutamate to excessive synaptic efficacy

TL;DR: This review is a critical appraisal of the widespread assumption that high extracellular glutamate, resulting from enhanced pre-synaptic release superimposed on deficient uptake and/or cytosolic efflux, is the key to excessive glutamate-mediated excitation in neurological disorders.
Journal ArticleDOI

Twenty years of dendrotoxins.

TL;DR: The dendrotoxins have little or no anti-protease activity, but they were demonstrated to block particular subtypes of voltage-dependent potassium channels in neurons, and have become widely used as probes for studying the function of K(+) channels in physiology and pathophysiology.
Journal ArticleDOI

Neurotoxicity in Snakebite—The Limits of Our Knowledge

TL;DR: A uniform system of classification of the pattern of neuromuscular weakness and models for predicting type of toxicity and development of respiratory weakness are still lacking, and would greatly aid clinical decision making and future research.
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Glutamate-Based Antidepressants: Preclinical Psychopharmacology

TL;DR: Preclinical evidence that it may be possible to develop glutamate-based antidepressants by altering synaptic concentrations of glutamate via specialized transporters such as glial glutamate transporter 1 (excitatory amino-acid transporter 2) is reviewed.
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Relationships among seizures, extracellular amino acid changes, and neurodegeneration induced by 4-aminopyridine in rat hippocampus : A microdialysis and electroencephalographic study

TL;DR: It is concluded that the glutamate release‐inducing effect of 4‐aminopyridine results in excitotoxicity because it occurs at the level of nerve endings, thus permitting the interaction of glutamate with its postsynaptic receptors, which is probably not the case after K+ depolarization.
References
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Journal ArticleDOI

The three-dimensional organization of the hippocampal formation: a review of anatomical data.

TL;DR: It is concluded that it is heuristically most reasonable to consider the hippocampal formation as a three-dimensional cortical region with important information processing taking place in both the transverse and long axes.
Journal ArticleDOI

2,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline: a neuroprotectant for cerebral ischemia.

TL;DR: NBQX protects against global ischemia, even when administered 2 hours after an ischemic challenge, and is a potent and selective inhibitor of binding to the quisqualate subtype of the glutamate receptor, with no activity at the NMDA and glycine sites.
Journal ArticleDOI

Anatomical distributions of four pharmacologically distinct 3H-L-glutamate binding sites

TL;DR: There are at least four distinct classes of 3H-L-glutamate binding sites which differ in their anatomical distribution, pharmacological profile and regulation by ions, and a third site may represent the KA receptor and a fourth binding site does not conform to present receptor classifications.
Journal Article

Excitotoxic mechanisms of epileptic brain damage.

TL;DR: It is found that the seizure-brain damage syndrome induced by cholinergic agents can be prevented by pretreatment with atropine and that the Syndrome induced by any of the above methods can be either prevented or aborted respectively by either pre- or posttreatment with diazepam.
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What will happen if your motor neurons are exposed to Dendrotoxin?

In conclusion, the present data on dendrotoxin K, together with the previously described pattern of neurotoxicity for alpha-dendrotoxin, show that these homologues act via different mechanisms and, thus, can be used effectively as complementary tools to study seizures and neuronal cell death.