HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Brown, D A Articles by Halliwell, J V Search for Related Content PubMed PubMed Citation Articles by Brown, D A Articles by Halliwell, J V

The effects of some cholinomimetic substances and their antagonists on the peak height of compound action potentials recorded from the terminal region of the habenulointerpeduncular pathway have been studied using a rat brain slice preparation. Carbachol and acetylcholine (ACh) depressed the peak height of the compound action potential and increased the latency to peak. The nicotinic agonists nicotine and dimethylphenylpiperazinium depressed the peak height of the compound action potential while muscarine and glutamate had no effect. The depressant effect of carbachol was blocked by the nicotinic antagonists hexamethonium, mecamylamine and d-tubocurarine but not by atropine. Physostigmine enhanced the effects of ACh and, to a lesser extent, carbachol. In the presence of physostigmine, carbachol or ACh initiated a spontaneous oscillation of the amplitude of the compound action potential which was Ca2+ dependent and was blocked by mecamylamine. It is concluded that depression of the amplitude of the compound action potential is due to activation of presynaptic nicotinic receptors. The results are discussed with reference to possible cholinergic mechanisms in the habenulointerpeduncular pathway.

This article has been cited by other articles:

				C. Lena and J.-P. Changeux Role of Ca2+ Ions in Nicotinic Facilitation of GABA Release in Mouse Thalamus J. Neurosci., January 15, 1997; 17(2): 576 - 585. [Abstract] [Full Text] [PDF]