d 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

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

Involvement of proprioceptive feedback in brainstem-triggered convulsions.

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OBJECTIVE In rodents, specific motor components of generalized convulsive seizures depend on two distinct anatomic substrates: (a) forebrain networks are responsible for facial and forelimb clonus with or without rearing and falling; and (b) brainstem networks are responsible for running-bouncing

Characterization of cholinergic regulation of seizures by the midline thalamus.

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This study determined the effects of injections of different cholinergic agents in the central medial intralaminar nucleus of the thalamus on seizures induced by intravenous injection of pentylenetetrazol. Injections of the cholinesterase inhibitor, neostigmine bromide, induced a stiff, tremulous

Potential of memantine, D-tubocurarine, and atropine in preventing acute toxic myopathy induced by organophosphate nerve agents: soman, sarin, tabun and VX.

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Male Sprague-Dawley rats when administered sc a sublethal dose of organophosphorus cholinesterase inhibitors such as the nerve agents, soman (100 micrograms/kg, sc), sarin (110 micrograms/kg, sc), tabun (200 micrograms/kg, sc), or VX (12 micrograms/kg, sc), developed seizures and severe muscle

Effects of apamin and nicotinic acetylcholine receptor antagonists on inferior collicular seizures.

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These studies compared the actions of apamin and nicotinic acetylcholine antagonists on seizure genesis within the inferior collicular cortex. In vitro alpha-bungarotoxin, d-tubocurarine and gallamine all competitively displaced [125I]apamin binding to brain sections through the inferior colliculus,

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