tubocurarine/seizures

Intracisternal (i. cist.) administration of d-tubocurarine (0.025-0. 100 mg. kg-1) in alpha-chloralose-anaesthetized dogs caused a dose-related increase in blood pressure associated with seizures. When injected in dogs pretreated with guanethidine (15 mg. i.v.), d-tubocurarine elicited the same

Mediation of nicotine-induced convulsions by central nicotinic receptors of the 'C6' type.

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The nature of the central receptors mediating the convulsant actions of nicotine has been investigated. Clonic tonic convulsions were seen in mice following intracerebroventricular (i.c.v.) injection of nicotinic agonists. (-)Nicotine was the most potent agonist tested, with a CD50 of 7.9 X 10(-9)

Antagonism of some central effects of d-tubocurarine by gamma-aminobutyric acid.

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d-Tubocurarine (dtc) administered intracerebroventricularly (icv) to rats produced seizures. Gamma-aminobutyric acid (GABA) administered icv or hydroxylamine administered intraperitoneally (ip) protected the rats from dtc-induced seizures. GABA administered (ip) was ineffective. Local application of

GABAergic systems modulate nicotinic receptor-mediated seizures in mice.

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The pharmacology of nicotinic receptor-mediated seizures was investigated in C3H mice. Eleven nicotinic agonists and six antagonists were administered centrally (i.c.v.). Epibatidine and epiboxidine were the most potent agonists tested, whereas acetylcholine and the alpha7*-selective compounds

Audiogenic seizures in curarized mice.

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Previous experiments have indicated that interference with somatosensory feedback from convulsive movements may lessen the severity of audiogenic seizures in susceptible rodents. For further investigation of this phenomenon, mice were partially immobilized with tubocurarine chloride to attenuate

Cerebrospinal fluid levels of d-tubocurarine in man.

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Using radioimmunoassay, d-tubocurarine (dTc) was found in the cerebrospinal fluid (CSF) of man after intravenous injection. When dTc was administered in a single dose (0.3 mg/kg) to nine patients, small quantities, 3.5 +/- .26 ng/ml (mean +/- SE), appeared in the lumbar CSF within 5 minutes. The

d-Tubocurarine causes neuronal death when injected directly into rat brain.

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d-Tubocurarine (d-TC) is a drug commonly used to produce muscle paralysis. Although it has been demonstrated to produce seizures when injected directly into the cerebral ventricles, no lasting neurotoxic effects have been reported. Data presented here suggest that amounts of d-TC as small as 1

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