4 amino butyric acid/infarction

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Diazepam does not reduce infarct size in rats subjected to transient occlusion of the middle cerebral artery when normothermia is maintained.

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Activation of the gamma-amino butyric acid (GABA)-ergic system might protect against the damage that occurs after cerebral ischaemia. We examined this hypothesis by administering diazepam to rats subjected to transient middle cerebral artery occlusion (MCAO) using the intraluminal thread method.

[Plasma amino acid concentrations and isoleucine-phenylalanine quotient in patients with acute myocardial infarct during amino acid infusion].

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OBJECTIVE The influence of substitution with two different amino acid solutions on changes in plasma amino acids were studied in patients with acute myocardial infarction. METHODS Thirty consecutive patients admitted to an intensive care unit were included in this open, nonrandomized study. The

[Metabolic changes in ischemic brain infarct].

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Serum and cerebrospinal fluid (CSF) from 17 patients less than 3 days after brain infarction (measurement 1) and during recovery 7 +/- 2 days after infarction (measurement 2) were analysed for organic acids (energy metabolites, keto acids and amino acids). Clinical parameters improved by 32% over

Extracellular amino acid changes in patients during reversible cerebral ischaemia.

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This study investigated the changes in extracellular chemistry during reversible human cerebral ischaemia. Delayed analysis was performed on samples taken from a subgroup of patients during aneurysm surgery previously reported. Frozen microdialysis samples from 14 patients who had all undergone

Estradiol alters only GAD67 mRNA levels in ischemic rat brain with no consequent effects on GABA.

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The present study tested the hypothesis that estradiol reduces tissue infarction after middle cerebral artery occlusion (MCAO) in estradiol-deficient females by augmenting glutamic acid decarboxylase (GAD) expression and thus activity, leading to increases in gamma-amino-butyric acid (GABA) tissue

Behavioral deficits and recovery following transient focal cerebral ischemia in rats: glutamatergic and GABAergic receptor densities.

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The neurobiologic mechanisms underlying the recovery process following stroke are poorly understood. The present study investigated glutamatergic and gamma-amino butyric acid (GABA)-ergic receptor densities following experimental stroke in rats exposed to different environmental housing or

Effect of ligustrazine on levels of amino acid neurotransmitters in rat striatum after cerebral ischemia-reperfusion injury.

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This study aimed to evaluate the effect of ligustrazine on levels of amino acid transmitters in the extracellular fluid of striatum following cerebral ischemia/reperfusion (I/R) in male Sprague-Dawley rats. A microdialysis cannula guide was implanted into the right striatum. After recovery, animals

Phasic GABA signaling mediates the protective effects of cTBS against cerebral ischemia in mice.

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Continuous theta burst stimulation (cTBS) has been widely recognized as a therapeutic treatment for ischemic stroke, but the underlying mechanism is still elusive. Here, we investigated the protective effects of cTBS in the posterior parietal cortex during the chronic phase of stroke in the

Gua Lou Gui Zhi decoction attenuates post‑stroke spasticity via the modulation of GABAB receptors.

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The aim of the present study was to investigate the mechanisms underlying the neuroprotective and antispastic effects of Gua Lou Gui Zhi decoction (GLGZD) in a rat model of middle cerebral artery occlusion (MCAO). The MCAO rats were treated with GLGZD (14.3 g/kg body weight) once a day for a period

The Delta-Subunit Selective GABA A Receptor Modulator, DS2, Improves Stroke Recovery via an Anti-inflammatory Mechanism.

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Inflammatory processes are known to contribute to tissue damage in the central nervous system (CNS) across a broad range of neurological conditions, including stroke. Gamma amino butyric acid (GABA), the main inhibitory neurotransmitter in the CNS, has been implicated in modulating peripheral immune

Increased Susceptibility to Ischemic Brain Injury in Neuroplastin 65-Deficient Mice Likely via Glutamate Excitotoxicity.

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Cell adhesion molecules (CAMs) are involved in synaptic plasticity and neuronal survival in the adult brain. Neuroplastin 65 (Np65), one member of the immunoglobulin superfamily of CAMs, is brain-specific and highly expressed in rodent forebrain. The roles of Np65 in synaptic plasticity have been

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