Citalopram and 8-OH-DPAT attenuate nicotine-induced excitation of central noradrenaline neurons.
Previous electrophysiological studies have demonstrated that nicotine, intravenously administered, excites noradrenergic neurons in the locus coeruleus (LC) indirectly by releasing excitatory amino acids (EAA). In the present study the excitatory action of nicotine was inhibited by treatment with the selective 5-HT re-uptake inhibitor citalopram or the 5-HT1A receptor agonist 8-OH-DPAT. It is proposed that the antagonism between nicotine and citalopram or 8-OH-DPAT reflects an interaction between endogenous EAA, e.g. glutamate, and 5-HT. The results may, on a cellular basis, explain the attributed effectiveness of drugs that facilitate serotonergic neurotransmission in promoting smoking cessation.
Engberg
G
G
Department of Pharmacology, University of Göteborg, Sweden.
D017371:8-Hydroxy-2-(di-n-propylamino)tetralin / Q000494:pharmacology*; D000596:Amino Acids / Q000502:physiology; D000818:Animals; D015283:Citalopram / Q000494:pharmacology*; D007275:Injections, Intravenous; D008125:Locus Coeruleus / Q000187:drug effects*; D008297:Male; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D009538:Nicotine / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D009638:Norepinephrine / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012701:Serotonin / Q000502:physiology
D000596:Amino Acids; D015283:Citalopram; D012701:Serotonin; D009538:Nicotine; D017371:8-Hydroxy-2-(di-n-propylamino)tetralin; D009638:Norepinephrine