A comparison of the effects of meptazinol and morphine on the release of acetylcholine from slices of mouse cerebral cortex

Ennis, Christine; Stephens, R.J.

doi:10.1016/0028-3908(84)90085-6

Cited by 9 publications

(3 citation statements)

References 4 publications

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“…Mihfily et al presynaptic opiate receptors which might regulate the transmitter release (Hagan and Hughes, 1984). Similar molecular mechanisms might increase the release of acetylcholine in central cholinergic axons (Ennis and Stephens, 1984).…”

Section: Introductionmentioning

confidence: 98%

Naltrexone potentiates 4-aminopyridine seizures in the rat

Mihály

Bencsik

Solymosi

1990

J. Neural Transmission

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The effects of a pharmacological blockade of the mu opiate receptors on the manifestation of tonic-clonic seizures were investigated in freely moving animals. 4-aminopyridine, a specific blocker of the neuronal K+ channels was used to produce generalized convulsions. After pretreatment of adult rats with 1 mg/kg naltrexone HCl, 3, 5, 7, 9, 14 mg/kg 4-aminopyridine was injected intraperitoneally, and the latencies of the symptoms generated by 4-aminopyridine were measured. Naltrexone HCl decreased these latencies and enhanced the seizures significantly. The experiments provided further evidence for the existence of a tonic anticonvulsant opioid system in the brain.

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Section: Introductionmentioning

confidence: 98%

Naltrexone potentiates 4-aminopyridine seizures in the rat

Mihály

Bencsik

Solymosi

1990

J. Neural Transmission

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“…Their exact nature and function is, however, far from c1ear. In slices ofmouse cortex, morphine has been reported to increase acetylcholine release (Ennis and Stephens, 1984), while in slices of rat cortex, morphine inhibited acetylcholine release (Ennisand Wyllie, 1984). Both effects, whieh were mediated through !…”

Section: Brileymentioning

confidence: 99%

Biochemical Strategies in the Search for Cognition Enhancers

Briley

1990

Pharmacopsychiatry

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Memory is a complex multi-event procedure which is profoundly influenced by the overall psychological state. It is thus evident that there cannot be a "memory transmitter" and that many neurotransmitter systems are implicated in different parts of the cognitive process. In general, memory effects resulting from manipulation of the catecholamine systems are a reflection of altered arousal. Modification of cholinergic transmission or that of certain neuropeptides such as vasopressin would appear, however, to involve more directly the memory process itself. This article presents a brief overview of the part played by various neurotransmitter systems in cognitive function and suggests a number of research strategies by which new cognition enhancers may be sought.

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“…The mechanisms involved in this cholinergic effect are unclear as meptazinol was thought to lack anticholhesterase properties (Stephens et a1 1978), but more recent work has shown that cholinesterase is inhibited (Galli 1985;Strahan et a1 1985), the (-)-enantiomer being about 100 times less potent than physostigmine (Ennis et a1 1986). In addition it has been reported that meptazinol is able to increase the K+-evoked overflow of tritium from mouse cortical slices previously incubated with [3H]choline (Ennis & Stephens 1984) but it is uncertain if this is a consequence of cholinesterase inhibition or a reflection of an ability of meptazinol to increase the "euronal release of acetylcholine itself.…”

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confidence: 99%

An investigation of the mechanism involved in the cholinergic action of meptazinol

Hetherington

Hughes

Lees

1987

Journal of Pharmacy and Pharmacology

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In concentrations above 20 p~, (k)-meptazinol produced a contraction of the guinea-pig isolated ileum and this effect was antagonized by atropine (0.01 to 0.3 p~) in a manner which was not competitive. Cooling the preparation to 15°C blocked the contractile action of meptazinol and of dimethylphenylpiperazinium (DMPP) but did not affect the action of carbachol. Twitch responses of the rat phrenic nerve-diaphragm preparation induced by indirect electrical stimulation in the presence of naloxone (20 nM) were potentiated by meptazinol (1 to 40 p~) which also reversed a partial blockade of the twitch induced by tubocurarine. Neither of these effects was seen in tissues which had been pretreated with the cholinesterase inhibitor BW284C51 (0.2 p~) though tetraethylammonium iodide 40 p~ was still able to enhance the responses to stimulation. In the presence of naloxone r j 20 nM electrically induced responses of the rat isolated rectum were abolished by cinchocaine (10 p~), partially blocked by atropine (0.1 to 0.4 VM) and potentiated by meptazinol (1 to 30 p~). The latter action was not seen when meptazinol was administered in the presence of BW284C51. It is concluded that the cholinergic action of meptazinol in these tissues is due to an indirect effect, probably involving inhibition of cholinesterase and that no evidence was seen of any ability to increase the release of acetylcholine itself.

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A comparison of the effects of meptazinol and morphine on the release of acetylcholine from slices of mouse cerebral cortex

Cited by 9 publications

References 4 publications

Naltrexone potentiates 4-aminopyridine seizures in the rat

Naltrexone potentiates 4-aminopyridine seizures in the rat

Biochemical Strategies in the Search for Cognition Enhancers

An investigation of the mechanism involved in the cholinergic action of meptazinol

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