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Journal ArticleDOI

Transient reduction of cerebral blood flow leads to longlasting increase in GABA content in vulnerable structures and decreased susceptibility to bicuculline induced seizures.

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TLDR
The present results suggest that BCCA produces a longlasting increase in GABA content and as a consequence protection from bicuculline-induced seizures.
Abstract
Rats were exposed for 24 min to bilateral clamping of the common carotid arteries (BCCA) in pentobarbital anaesthesia. The GABA content was measured 24 hours, 48 hours, 4 days, 14 days and 3 months after BCCA. In other groups of rats seizures were elicited by i.p. injection of (+)-bicuculline (3 mg/kg) 24 hours, 48 hours, 4 days, 14 days and 3 months after BCCA. Analysis of the GABA content revealed significant increase compared with controls in the hippocampus, frontal cortex and substantia nigra from 24 hours up to 3 months. Bicuculline treatment induced tonic/clonic seizures and status epilepticus in sham operated animals; these effects were drastically diminished at various time points after BCCA. The present results suggest that BCCA produces a longlasting increase in GABA content and as a consequence protection from bicuculline-induced seizures.

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Preconditioned resistance to oxygen-glucose deprivation-induced cortical neuronal death: alterations in vesicular GABA and glutamate release

TL;DR: It is predicted that presynaptic alterations, specifically enhanced GABA release together with reduced glutamate release, may be important mediators of ischemic preconditioning, but suggest caution in regard to interventions aimed at increasing GABA(A) receptor activation.
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Effects of cadmium on memory processes in mice exposed to transient cerebral oligemia

TL;DR: Results indicate that cerebral oligemic hypoxia may alter cadmium neurotoxicity and potentiate the tendency for Cadmium-induced memory impairments in the passive avoidance task and spontaneous alternation deficits.
Journal ArticleDOI

Hypoxia protects against the neurotoxicity of kainic acid.

TL;DR: It is shown that a protective mechanism induced by hypoxia may affect the glutamatergic transmission in these synapses and prevent excessive synaptic excitation, and the possible involvement of adenosine and/or GABA in this protective mechanism is discussed.
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The role of opioid receptors in hypoxic preconditioning against seizures in brain.

TL;DR: Evidence is provided that mu- and kappa-opioid receptors are involved in HPC against seizures in the brain against pentylenetetrazol induced convulsions.
Journal ArticleDOI

Transient hyperthermia protects against subsequent seizures and epilepsy-induced cell damage in the rat

TL;DR: It is found that moderate transient hyperthermic preconditioning markedly reduced kainic-acid-induced neuronal cell loss and attenuated susceptibility to bicuculline-induced seizures and this protection lasted about 1 week and peaked 3 to 5 days after pretreatment.
References
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Journal ArticleDOI

Modification of seizure activity by electrical stimulation. II. Motor seizure.

TL;DR: It was found that the development of motor seizures by stimulation of the amygdala resulted in an increased ability of the contralateral amygdala, and the septal area, but not of the hippocampus, to drive motor seizures when stimulated (“transfer”).
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Temporal profile of neuronal damage in a model of transient forebrain ischemia.

TL;DR: The unique delay in onset of ischemic cell change and the protracte increase in its incidence between 24 and 72 hours could reflect either delayed‐appearance of isChemic change in previously killed neurons or a delayed insult that continued to jeopardize compromised but otherwise viable neurons during the postischemic period.
Journal ArticleDOI

Modification of seizure activity by electrical stimulation: III. Mechanisms

TL;DR: It was found that stimulation of more than one area increases the rate of seizure development, whereas disrupting inter-limbic connections retards seizure development.
Journal ArticleDOI

The density and distribution of ischemic brain injury in the rat following 2–10 min of forebrain ischemia

TL;DR: Mild brain damage was observed in some animals already after 2 min, and more consistently after 4 min of ischemia, and selective neuronal necrosis of the cerebral cortex worsened into infarction after higher doses of insult.
Journal ArticleDOI

Selective vulnerability of the hippocampus in brain ischemia.

TL;DR: *Department of Neurophysiology, Institute of Physiology, Medical Faculty, Ruhr-Universitlt Bochum, and MRC Anatomical Neuropharmacology Unit, _ Department of Pha-rmacology, University of Oxford, Oxford, U.K.R.G.
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