α2-Null mutant mice have altered levels of neuronal activity in restricted midbrain and limbic brain regions during nicotine withdrawal as demonstrated by cfos expression.

摘要: Neuronal nicotinic acetylcholine receptors (nAChRs) are the primary binding sites for nicotine within brain. Using alpha(α)2 nAChR subunit-null mutant mice, current study evaluates whether absence of this gene product during mecamylamine-precipitated withdrawal eliminates neuronal activity selective midbrain and limbic brain regions, as determined by expression immediate early gene, cfos. Our results demonstrate that enhances interpeduncular nucleus dorsal hippocampus, which is absent in mice null α2-containing nAChRs. In contrast, we observe α2-null exhibit a suppression dentate gyrus undergoing withdrawal. Interestingly, display potentiated specifically stratum lacunosum moleculare layer independent Overall, our findings have altered cfos distinct populations neurons structures mediate baseline withdrawal-induced activity.