subunits produced in MHb are predominately incorporated into α5* nAChRs expressed presynaptically on afferents to IPN. Second, injections of the Lenti-CHRNA5 vector into MHb rescued local α5 subunit mRNA expression, but not deficits in MHb 86Rb+ efflux. This suggests that nAChR signaling in MHb may be derived from α5* nAChRs located presynaptically on afferent inputs from brain sites not infected by the virus. Third, whilst the Lenti-CHRNA5 vector attenuated the deficits in nAChR signaling detected in IPN of knockout mice, this rescue was only partial (Fig. 2e). Hence, postsynaptically localized α5* nAChRs on IPN neurons, or perhaps presynaptic α5* nAChRs on afferent inputs that originate from brain sites other than the MHb, also play a major role in nAChR transmission in the IPN.
