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Blockade of the reward‐potentiating effects of nicotine on lateral hypothalamic brain stimulation by chlorisondamine
Author(s) -
Wise Roy,
Marcangione Caterina,
Bauco Pat
Publication year - 1998
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199805)29:1<72::aid-syn6>3.0.co;2-8
Subject(s) - nicotine , chlorisondamine , brain stimulation reward , stimulation , neuroscience , nicotinic agonist , brain stimulation , dopaminergic , dopamine , psychology , cholinergic , pharmacology , receptor , medicine , nucleus accumbens , blood pressure
Chlorisondamine, a quarternary nicotinic antagonist, was given in a dose that crosses the blood–brain barrier, is taken up and concentrated intracellularly by dopaminergic neurons, and induces long‐term blockade of the locomotor stimulant and rewarding effects of nicotine. This treatment had no effect on the rewarding effects of lateral hypothalamic brain stimulation, failing to shift the function that relates reward strength to rate of responding (rate–frequency function). That the treatment regimen was sufficient to block nicotinic receptors in the reward system was confirmed by the fact that it completely blocked the ability of normally effective nicotine to potentiate the rewarding effects of stimulation (shift this function to the left). These data add evidence that the direct, endogenous cholinergic contribution to brain stimulation reward is muscarinic and fit with other evidence that the potentiation of brain stimulation reward by exogenous nicotine involves actions on nicotinic receptors native to dopaminergic neurons. Synapse 29:72–79, 1998. © 1998 Wiley‐Liss, Inc.