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Attenuation of conflict‐induced suppression by clonidine: Indication of anxiolytic activity
Author(s) -
Kruse Hansjoerg,
Dunn Robert W.,
Theurer Karin L.,
Novick William J.,
Shearman Gary T.
Publication year - 1981
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430010206
Subject(s) - clonidine , phenoxybenzamine , yohimbine , anxiolytic , methysergide , chemistry , (+) naloxone , stimulation , locus coeruleus , phentolamine , endocrinology , anxiogenic , atropine , medicine , pharmacology , propranolol , antagonist , central nervous system , receptor
Clonidine was tested in a conflict‐induced suppression paradigm (bar pressing for food reward suppressed by electric foot shock) in rats. This drug significantly and dose dependently (25–100 μg/kg) both increased punished responding and decreased unpunished responding. Clonidine at 200 μg/kg had no effect on punished bar pressing, although it markedly inhibited unpunished responding due to sedation. The effect of clonidine on shock‐suppressed lever pressing was prevented by yohimbine 5 mg/kg and partially antagonized by phenoxybenzamine 2.5 mg/kg but was not significantly altered by phenoxybenzamine 1 mg/kg, atropine 5 mg/kg, methysergide 5 mg/kg, or naloxone 10 mg/kg. This activity of clonidine does not seem to be due to its analgesic or food intake‐increasing properties. It may be a true anxiolytic effect, brought about by presynaptic stimulation of noradrenergic neurons which could result in an inhibitory influence on the locus coeruleus.