A Re‐evaluation of Acetylcholine Receptors on Feline Renshaw Cells

King, Katie; Ryall, R. W.

doi:10.1111/j.1476-5381.1981.tb10442.x

Cited by 18 publications

(2 citation statements)

References 9 publications

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“…neurones seem similar to Renshaw cells (Curtis & Ryall, 1966;King & Ryall, 1981) or sympathetic ganglion cells (Volle, 1966) in terms of their cholinergic responsiveness, having both nicotinic and muscarinic components. In contrast to ganglionic or Renshaw cells, however, synaptic responses were not blocked by doses of nicotinic antagonists or atropine or both in excess of those required to completely abolish post-synaptic responses ofthe same neurone to cholinomimetic agonists.…”

Section: Discussionmentioning

confidence: 99%

Chemical transmission in the rat interpeduncular nucleus in vitro.

Brown¹,

Docherty²,

Halliwell³

1983

The Journal of Physiology

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SUMMARY1. We have used a rat brain-slice preparation to study the effects of some cholinomimetic and amino acid agonists and antagonists on the discharge frequency of neurones in the interpeduncular nucleus (i.p.n.), and on the response of these neurones to electrical stimulation of their main excitatory input, the fasciculus retroflexus of Meynert (f.r.m.).2. A high proportion of i.p.n. neurones were excited by carbachol, acetylcholine (ACh) and muscarine, but methacholine was less effective. The amino acids L-glutamate and L-aspartate were highly effective stimulants of i.p.n. neurones.3. The responses to ACh or carbachol were greatly reduced by the nicotinic blocking agents hexamethonium, d-tubocurarine and mecamylamine but only slightly reduced by atropine. The response to muscarine was abolished by low doses of atropine. a-Bungarotoxin did not block the response of i.p.n. neurones to f.r.m. stimulation or to cholinomimetic agonists. 4. The response of i.p.n. neurones to f.r.m. stimulation was not appreciably affected by high doses of nicotinic antagonists or atropine nor was there any enhancement of the response by physostigmine.5. The amino acid antagonists y-D-glutamylglycine (yDGG) and 2-aminophosphonovalerate (2-APV) were effective blockers ofthe response to f.r.m. stimulation and preferentially reduced responses to aspartate while having little effect on responses to glutamate or cholinomimetic agonists.6. It is concluded that ACh is an unlikely candidate for transmitter in this pathway despite abundant neurochemical evidence in its favour. It is more likely that the transmitter is an excitatory amino acid, probably an aspartate-like substance.

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Section: Discussionmentioning

confidence: 99%

Chemical transmission in the rat interpeduncular nucleus in vitro.

Brown¹,

Docherty²,

Halliwell³

1983

The Journal of Physiology

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“…We used this derivative of atropine in the anticipation that we would limit diffusion relative to the more lipid-soluble and highly diffusible tertiary derivative (Brezenoff et al, 1988). In retrospect, and in knowing of the role of nicotinic receptors in the cocaine response (see below), it is possible that the quaternary methylbromide compound may have produced a partial blockade of local nicotinic receptors as has been suggested for peripheral nicotinic sites (King and Ryall, 1981).…”

Section: Discussionmentioning

confidence: 99%

The Importance of Brainstem Cholinergic Neurons in the Pressor Response to Cocaine

Buccafusco¹,

Davis²,

Shuster³

et al. 2004

J Pharmacol Exp Ther

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After intracisternal injection, 140 nmol (48 g) of cocaine (but not lidocaine or procaine) evoked an increase in mean arterial pressure (MAP) of 41 mm Hg. The increase in MAP began within 1 min after injection and lasted 10 to 15 min. The pressor response to intracisternal injection of cocaine was not mediated through central ␣-adrenergic receptors, but intracisternal pretreatment with D1 or D2 dopamine receptor antagonists shortened the duration of the response. Pretreatment with intracisternal injection of hemicholinium-3 to deplete medullary acetylcholine produced a dose-dependent inhibition of the pressor and tachycardic responses to intracisternal injection of cocaine. Central pretreatment with hemicholinium-3 also inhibited the pressor response to intravenous injection of 0.5 mg/kg cocaine. Atropine pretreatment was only partly effective in blocking the pressor and tachycardic responses to intracisternal injection of cocaine. However, a single intracisternal injection of the nicotinic ganglionic receptor blocker hexamethonium inhibited the pressor response to cocaine administered intracisternally 24 h later, and on each of the following 4 days. The blocking effect of hexamethonium was not mimicked by the ␣7 selective antagonist methyllycaconitine or by the ␣4␤2 subtype-preferring antagonist dihydro-␤-erythroidine. The data suggest that the pressor response to cocaine is mediated by medullary acetylcholine release on to nicotinic receptors of the ganglionic type, enhancing the output of bulbospinal sympathetic premotor neurons. Our results provide new evidence for the prolonged inactivation of relevant central nicotinic receptors by nicotinic receptor antagonists, and suggest that such compounds might be used safely for cocaine overdose, as well as for antiabuse issues without the concern for autonomic side effects.The ability of cocaine to increase systemic blood pressure usually is considered to be commensurate with drug's pharmacological classification as an indirect-acting sympathomimetic amine. Whereas cocaine conforms to this classification both in the peripheral and central nervous systems, the role of the CNS in terms of blood pressure alterations has been debated (Knuepfer et al., 1993;Gillis et al., 1995;Bernards, 1996). In fact, agonists at central ␣ 2 -adrenergic receptors such as clonidine and ␣-methyldopa are effective antihypertensive drugs; and levodopa and other dopaminergic antiParkinson agents often produce orthostatic hypotension as a side effect. Also, systemic administration of cocaine has been reported to decrease sympathetic nervous activity (Knuepfer and Branch, 1992;Gillis et al., 1995;Abrahams et al., 1996). Yet, there have been instances when cocaine has been administered directly into the CNS, usually via the cerebrospinal fluid, that the drug elicits an increase in arterial blood pressure. However, based upon the requirement for relatively high doses to elicit a pressor response via the lateral ventricular route (Knuepfer et al., 1993), it is unlikely that forebrain str...

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Modulation of Cholinergic Transmission by Substance P

Ryall

1982

Novartis Foundation Symposia

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A Re‐evaluation of Acetylcholine Receptors on Feline Renshaw Cells

Cited by 18 publications

References 9 publications

Chemical transmission in the rat interpeduncular nucleus in vitro.

Chemical transmission in the rat interpeduncular nucleus in vitro.

The Importance of Brainstem Cholinergic Neurons in the Pressor Response to Cocaine

Modulation of Cholinergic Transmission by Substance P

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