picrotoxin/iskemia

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Optical imaging of hippocampal neurons with a chloride-sensitive dye: early effects of in vitro ischemia.

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We determined if changes in intraneuronal Cl- occur early after ischemia in the hippocampal slice. Slices from juvenile rats (14-19 days old) were loaded with the cell-permeant form of 6-methoxy-N-ethylquinolinium chloride (MEQ), a Cl(-)-sensitive fluorescent dye. Real-time changes in intracellular

Effects of calcium-channel blockers on picrotoxin-induced centrogenic arrhythmias in cats.

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Intravenous picrotoxin injection has been established as a model of producing arrhythmias, mainly through enhanced central sympathetic outflow. The effects of calcium-channel blockers, and a beta-blocker on these arrhythmias were tested in chloralose-anesthetized cats. Picrotoxin (10 mg/kg, i.v.)

Gasping is elicited by briefer hypoxia or ischemia following blockade of glycinergic transmission.

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The 'switching model' for generation of respiratory rhythms holds that gasping represents the release of a rostral medullary pacemaker mechanism from the pontomedullary neuronal circuit that generates eupnea. In a perfused preparation of the decerebrate juvenile rat, exposure to ischemia or

Neuroprotective efficacy of AR-A008055, a clomethiazole analogue, in a global model of acute ischaemic stroke and its effect on ischaemia-induced glutamate and GABA efflux in vitro.

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We have investigated the neuroprotective properties of AR-A008055 [(+/-)-1-(4-methyl-5-thiazolyl-1-phenyl-methylamine], a novel compound structurally related to clomethiazole. Administration (i.p.) of (+/-)-AR-A008055 60 min after 5 min of global cerebral ischaemia in gerbils produced a

Role of GABA in electro-acupuncture therapy on cerebral ischemia induced by occlusion of the middle cerebral artery in rats.

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This study investigated the possible involvement of gamma-aminobutyric acid (GABA) in the therapeutic effect of cerebral ischemia by electro-acupuncture (EA) using the rat model with middle cerebral artery occlusion (MCAO). By immunohistochemistry, the changes of GABA expression level in the primary

Forebrain ischemia: effect on pharmacologically induced seizure thresholds in the rat.

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Seizures are common after severe cerebral ischemia. To examine the mechanisms underlying these seizures, we determined the impact of prior forebrain ischemia on the seizure thresholds of four convulsants with differing modes of action: lidocaine, pentylenetetrazol (PTZ), N-methyl-D-aspartate (NMDA),

Role of GABAergic activity of sodium valproate against ischemia-reperfusion-induced acute kidney injury in rats.

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Gamma amino butyric acid (GABA) has been reported to be renoprotective in various preclinical studies. Sodium valproate (SVP) is documented to protect against renal injury through its histone deacetylase-inhibiting activity. The present study investigated the involvement of GABAA receptors and the

Effects of microinjection of picrotoxin into posterior hypothalamus on ventricular electric stability.

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Ventricular fibrillation threshold (VFT), serum potassium, and monophasic action potentials (MAP) have been assessed before and after microinjection of picrotoxin (Pic) into posterior hypothalamus in rabbits. Pic (2 and 3 micrograms) brought about a biphasic effect on VFT, an initial decrease

On the regulation of ischaemia-induced glutamate efflux from rat cortex by GABA; in vitro studies with GABA, clomethiazole and pentobarbitone.

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Prisms of adult rat cortex were maintained in vitro in either aerobic conditions (control) or conditions simulating an acute ischaemic challenge (hypoxia with no added glucose). Endogenous glutamate efflux increased with time in ischaemic conditions, being 2.7 fold higher than control efflux at 45

Functional integration of newly generated neurons into striatum after cerebral ischemia in the adult rat brain.

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OBJECTIVE Ischemic injury can induce neurogenesis in the striatum. Those newborn neurons can express glutamic acid decarboxylase and choline acetyltransferase, markers of GABAergic and cholinergic neurons, respectively. The present study investigated whether these GABAergic and cholinergic new

Diazepam promotes ATP recovery and prevents cytochrome c release in hippocampal slices after in vitro ischemia.

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Benzodiazepines protect hippocampal neurons when administered within the first few hours after transient cerebral ischemia. Here, we examined the ability of diazepam to prevent early signals of cell injury (before cell death) after in vitro ischemia. Ischemia in vitro or in vivo causes a rapid

The chloride transporter Na(+)-K(+)-Cl- cotransporter isoform-1 contributes to intracellular chloride increases after in vitro ischemia.

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Ischemic episodes in the CNS cause significant disturbances in neuronal ionic homeostasis. To directly measure changes in intracellular Cl- concentration ([Cl-]i) during and after ischemia, we used Clomeleon, a novel ratiometric optical indicator for Cl-. Hippocampal slices from adult transgenic

Existence of a powerful inhibitory mechanism in the medial region of caudal medulla--with special reference to the paramedian reticular nucleus.

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Inhibitory actions of the medial trigon of the caudal medulla (ITM) with special reference to the paramedian reticular nucleus (PRN) were explored in cats under chloralose (40 mg/kg) and urethane (400 mg/kg) anesthesia. Stimulation with square wave pulses (80 Hz, 1 msec, 100-200 microA) produced a

Synthetic oxytocin as an antagonist of experimental cardiac anoxic changes in rabbits.

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Synthetic oxytocin (Syntocinon) can be shown to reduce or abolish ST-T changes induced experimentally by hypoxaemia alone, by hypoxaemia and ergometrine, by vasopressin, and by a new procedure involving injection of small doses of picrotoxin into the lateral cerebral ventricle. Ventricular

Neurogenesis of gasping does not require inhibitory transmission using GABA(A) or glycine receptors.

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We evaluated the hypothesis that the neurogenesis of gasping is not dependent upon inhibitory synaptic transmission involving GABA(A) or glycine receptors. Activity of the phrenic nerve was recorded in a perfused juvenile rat preparation. The pattern of phrenic activity was altered from eupnea to

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