1969
DOI: 10.1007/bf00403709
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Antagonism by antimuscarinic and ganglion-blocking drugs of some of the behavioural effects of nicotine

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Cited by 43 publications
(13 citation statements)
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“…Such motor disturbances may account for the initial depressant actions of nicotine that have been observed in a variety of testing procedures (e.g. Morrison et al, 1969;Pradhan & Bowling, 1971). Small intravenous doses of nicotine markedly suppress spinal reflexes (Schweitzer & Wright, 1938).…”
Section: Discussionmentioning
confidence: 99%
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“…Such motor disturbances may account for the initial depressant actions of nicotine that have been observed in a variety of testing procedures (e.g. Morrison et al, 1969;Pradhan & Bowling, 1971). Small intravenous doses of nicotine markedly suppress spinal reflexes (Schweitzer & Wright, 1938).…”
Section: Discussionmentioning
confidence: 99%
“…Hence, nicotine appears to act at a central site to produce hyperactivity, in common with certain other behavioural actions (e.g. Morrison et al, 1969;Spealman, Goldberg & Gardner, 1981). In vitro studies suggest that mecamylamine directly blocks nicotinic cholinoceptors, at least at autonomic ganglia (Ascher, Large & Rang, 1979).…”
Section: Discussionmentioning
confidence: 99%
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“…The results obtained in this study are agreement with previous reports (Stolerman, Fink, & Jarvik, 1973) (Clarke & Kumar, 1983) that locomotor stimulant effects were developed at low dose of nicotine, followed by a decrease at high dose of nicotine in its locomotor depressant effects, which is governed centrally mediated theoretically (Morrison et al, 1969). The sensitized nicotine group (0.5 N) travelled longest in locomotor activity among all the nicotine test groups, which is supported by…”
Section: Assessment Of Bioactivity Of Nano-nicotine Via Locomotor Tessupporting
confidence: 92%
“…Short term exposure to nicotine could stimulate central nervous system neurohumoral pathways through activation of nicotinic receptors, causing release of acetylcholine, dopamine, norepinephrine, serotonin (N. L. Benowitz, 1988). Exposure to nicotine develops a biphasic dose-response relation: low doses of nicotine cause ganglionic stimulation, while high dose of nicotine causes ganglionic depression (Morrison, Goodyear, & Sellers, 1969). The biphasic effects are noted that at low dose of nicotine, cardiovascular effects are mediated by increasing blood pressure and heart rate via the central nervous system; on the other hand, at high dose of nicotine, ganglionic stimulation is mediated from peripheral nervous system.…”
Section: Historical Backgroundmentioning
confidence: 99%