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bicuculline/necrose
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Histamine protects against NMDA-induced necrosis in cultured cortical neurons through H receptor/cyclic AMP/protein kinase A and H receptor/GABA release pathways.
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Using histamine and the H3 receptor antagonist thioperamide, the roles of histamine receptors in NMDA-induced necrosis were investigated in rat cultured cortical neurons. Within 3 h of intense NMDA insult, most neurons died by necrosis. Histamine reversed the neurotoxicity in a
Thiopental inhibits tumor necrosis factor alpha-induced activation of nuclear factor kappaB through suppression of kappaB kinase activity.
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BACKGROUND
Thiopental is frequently used for the treatment of intracranial hypertension after severe head injury and is associated with immunosuppressive effects. The authors have recently reported that thiopental inhibits activation of nuclear factor (NF) kappaB, a transcription factor implicated
Bicuculline methiodide attenuates hepatic injury and decreases mortality in septic rats: role of cytokines.
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Bicuculline methiodide attenuates inflammation by inhibiting the production of proinflammatory cytokines, such as tumor necrosis factor-alpha, and by increasing the production of the anti-inflammatory cytokine interleukin-10, both of which play important roles in the pathogenesis of sepsis. The aim
Tumor necrosis factor reduces the amplitude of rat cortical spreading depression in vivo.
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OBJECTIVE
Brain damage and ischemia often trigger cortical spreading depression (CSD), which aggravates brain damage. The proinflammatory cytokine tumor necrosis factor (TNF) is significantly upregulated during brain damage, but it is unknown whether TNF influences spreading depression in cerebral
The histamine H3 receptor antagonist clobenpropit enhances GABA release to protect against NMDA-induced excitotoxicity through the cAMP/protein kinase A pathway in cultured cortical neurons.
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Using the histamine H3 receptor antagonist clobenpropit, the roles of histamine H3 receptors in NMDA-induced necrosis were investigated in rat cultured cortical neurons. Clobenpropit reversed the neurotoxicity in a concentration-dependent manner, and showed peak protection at a concentration of
In vivo studies of GABAergic effects in experimental hepatic encephalopathy.
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The GABAergic agonist, muscimol, and antagonists, picrotoxin and bicuculline, have been studied in rats with chronic portacaval shunts and in rats developing hepatic encephalopathy after massive ischemic necrosis due to hepatic artery ligation within 48 hr of a portacaval shunt. After the chronic
Biphasic effects of baicalin, an active constituent of Scutellaria baicalensis Georgi, in the spontaneous sleep-wake regulation.
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OBJECTIVE
Baicalin is an active compound originating from the root of Scutellaria baicalensis Georgi, which has been used for anti-inflammation, anti-bacteria, anti-hypertension, anti-allergy and sedation since ancient China, though the neuronal mechanisms involved in the sedative effect is still
Accumulation of GABAergic neurons, causing a focal ambient GABA gradient, and downregulation of KCC2 are induced during microgyrus formation in a mouse model of polymicrogyria.
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Although focal cortical malformations are considered neuronal migration disorders, their formation mechanisms remain unknown. We addressed how the γ-aminobutyric acid (GABA)ergic system affects the GABAergic and glutamatergic neuronal migration underlying such malformations. A focal freeze-lesion
Effects of adenosine and gamma-aminobutyric acid A receptor antagonists on N-methyl-D-aspartate induced neurotoxicity in the rat hippocampus.
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This study investigated the modulatory actions of adenosine and gamma-aminobutyric acid (GABA) on several aspects of N-methyl-D-aspartate (NMDA)-induced neurotoxicity, including neuronal loss, atrophy, necrosis, and calcium accumulation in the hippocampus. For this purpose, we combined unilateral
Effects of neonatal status epilepticus on rat brain development.
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A single, 2-hour episode of status epilepticus induced by flurothyl (1,500 mul) in 4-day-old rats irreversibly curtailed brain weight and brain DNA. Status epilepticus inhibited DNA synthesis but did not increase DNA breakdown and produced no histologic lesions. Rats with status epilepticus showed
[Relation between GLu-R and the protective effect of hypothermia on oxygen and glucose deprivation injury in hippocampal slice or rat].
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OBJECTIVE
To investigate the relation between Glu-R and the protective effect of hypothermia on oxygen and glucose deprivation (OGD) injury in hippocampal slices of rat.
METHODS
(1) We had established OGD injury model in rat hippocampal slices. The changes of orthodromic population spike(OPS) during
Study of the expression of GABA(A) receptor in rats during acute lung injury caused by endotoxin.
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The objective of the present study was to investigate the role of γ-aminobutyric acid type A receptor (GABA(A)R) in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Thirty-two male wistar rats were randomly divided into four groups. Rats in the GABA group were pretreated with LPS
Histogranin, a modified histone H4 fragment endowed with N-methyl-D-aspartate antagonist and immunostimulatory activities.
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Histogranin is a naturally-occurring pentadecapeptide with a structure 80% homologous with that a fragment-(86-100) of histone H4. First isolated from bovine adrenal medulla, the peptide was also shown to be present in the pituitary, brain, adrenal glands, blood plasma, lungs and spleen. At the
Sodium Valproate Improves Skin Flap Survival via Gamma-Aminobutyric Acid and Histone Deacetylase Inhibitory System.
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Sodium valproate interacts with biological systems through different mechanisms such as activation of gamma-aminobutyric acid (GABA)-sensitive chloride channels and inhibition of histone deacetylase. In this study, we examined the effect of sodium valproate in random-pattern skin flap of rats and
Stretchable microelectrode arrays--a tool for discovering mechanisms of functional deficits underlying traumatic brain injury and interfacing neurons with neuroprosthetics.
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Traumatic brain injury (TBI) can be caused by motor vehicle accidents, falls and firearms. TBI can result in major neurological dysfunction such as chronic seizures and memory disturbances. To discover mechanisms of functional deficits underlying TBI, we developed a stretchable microelectrode array
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