Effects of chronic nicotine administration and its withdrawal on striatal FosB/ΔFosB and c-Fos expression in rats and mice

Abstract

ΔFosB, a member of Fos family of transcription factors, is implicated in behavioural responses and synaptic plasticity induced by abused drugs. We studied the expressions of FosB/ΔFosB and c-Fos immunohistochemically in two dopaminergic brain areas, nucleus accumbens (NAcc) and caudate-putamen (CPu). In mice neither 2- nor 7-week oral nicotine treatment induced expression of long-lived ΔFosB isoforms although during the treatment in the NAcc FosB/ΔFosB expression was increased as was c-Fos in the CPu. In rats given nicotine subcutaneously once daily for 5 days FosB/ΔFosB expression was elevated in the NAcc still after 24-h withdrawal suggesting accumulation of ΔFosB but in the CPu neither FosB/ΔFosB nor c-Fos expression was altered. Thus, in rats repeated nicotine administration seems mainly affect the NAcc paralleling with the evidence that nicotine stimulates preferentially mesolimbic dopamine system. Also, repeated nicotine induced behavioural sensitization in rats agreeing with suggested role of ΔFosB in the development of psychomotor sensitization. However, in mice given nicotine via drinking fluid although striatal fosB and c-fos were activated by nicotine even after 7-week treatment no evidence of accumulation of long-lived ΔFosB was found suggesting perhaps a species difference or more likely a role for the manner of administration.