The influence of stress on psychopharmacological responses to nicotine.
This essay considers the mechanisms which may mediate the apparent anxiolytic properties of nicotine and which are thought to be responsible for the 'calming' effect of tobacco smoke experienced by many smokers. It summarizes the evidence that, in many tests for anxiolytic activity, the effects of nicotine do not resemble those of established anxiolytic drugs such as diazepam and concludes that it is likely that neural systems other than those which mediate the responses to the benzodiazepines are responsible for the putative anxiolytic properties of nicotine. Circumstantial evidence which suggests that the increase in mesolimbic dopamine secretion evoked by nicotine may not only be rewarding per se but may also contribute to the ability of the drug to alleviate the effects of stress is presented. The essay also summarizes results which suggest that chronic nicotine evokes changes in the mesolimbic dopamine system which resemble those seen in animals treated chronically with antidepressant drugs and proposes that the mechanisms which mediate the ability of antidepressant drugs to alleviate the effects of stress may also mediate the apparent anxiolytic properties of nicotine. The possible consequences of this hypothesis for future research are considered.
Balfour
D J
DJ
Department of Pharmacology and Clinical Pharmacology, University Medical School, Ninewells Hospital, Dundee, Scotland, UK.
D000818:Animals; D001143:Arousal / Q000187:drug effects*; D001921:Brain / Q000187:drug effects*; D003345:Corticosterone / Q000097:blood; D006801:Humans; D009538:Nicotine / Q000494:pharmacology*; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects; D011985:Receptors, Serotonin / Q000187:drug effects; D012907:Smoking / Q000503:physiopathology / Q000523:psychology*; D013315:Stress, Psychological / Q000150:complications*
D011954:Receptors, Dopamine; D011985:Receptors, Serotonin; D009538:Nicotine; D003345:Corticosterone