Altered synaptic transmission at olfactory and vomeronasal nerve terminals in mice lacking N-type calcium channel Cav2.2.

摘要: We investigated the role of voltage-activated calcium (Cav) channels for synaptic transmission at mouse olfactory and vomeronasal nerve terminals first synapse main accessory pathways, respectively. provided evidence a central N-type Cav channel subunit Cav2.2 in presynaptic transmitter release these synapses. Striking immunoreactivity was localised to glomerular neuropil bulb (MOB) (AOB), co-localised with molecules such as bassoon. Voltage-clamp recordings sensory nerve-evoked, excitatory postsynaptic currents (EPSCs) mitral/tufted (M/T) superficial tufted cells MOB mitral AOB, combination established subtype-specific toxins, indicated predominant synapses, whereas L-type, P/Q-type, R-type had either no or only relatively minor contributions. In Cacna1b mutant mice lacking (α1B) channels, nerve-evoked M/T cell EPSCs were not reduced but became blocker-resistant, thus indicating major reorganisation compensation subunits result deletion this synapse. Cav2.2-deficient also revealed that critically required paired-pulse depression MOB, they demonstrated an essential requirement AOB cells. Thus, loss-of-function mutations are unlikely cause general anosmia emerges strong candidate search causing altered perception, changes sensitivity social responses chemostimuli.