Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1992-12-17
pubmed:abstractText
Chick ciliary ganglion neurones were investigated by whole cell voltage clamp recordings. The ACh- or nicotine-induced inward current was partially inhibited by perfusing the neurones with 5-HT. This effect was rapid (< or = 1 min), dose-dependent (50-1000 microM) and quickly reversible. The selective 5-HT1A agonist 8-OH-DPAT (10 microM) reduced the nicotinic ACh response more potently, irrespective of the absence or presence of propranolol (1 microM), a known 5-HT1A antagonist. Other serotonergic antagonists, like ICS 205-930 (1 microM), mianserin (10 microM) and methysergide (10 microM), also failed to antagonize the 5-HT-mediated decrease in the nicotinic response. Muscarine (50 microM) did not affect the nicotine-induced inward current but the muscarinic agonist oxotremorine (10 microM) also decreased the nicotine-induced inward current. Atropine, at small concentrations failed to block this effect but caused some reduction of the ACh response itself at larger (1-10 microM) concentrations. It is suggested that 5-HT may modulate synaptic transmission in ciliary ganglion neurones in vivo. The site of action of 5-HT, oxotremorine and atropine might be at or close to the ACh receptor complex, because of the fast onset and reversibility of the effects and lack of specificity for structurally different drugs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0028-3908
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1001-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Inhibition of the nicotinic acetylcholine response by serotonergic and muscarinic agents in chick ciliary ganglion neurones.
pubmed:affiliation
Max-Planck-Institut für Physiologische, W.G. Kerckhoff-Institut, Bad Nauheim, Germany.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't