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Abstract
The accessory olfactory system is involved in processing pheromone signals and mediating stereotypical behaviors and neuroendocrine responses. Slice preparations of the murine accessory olfactory bulb (AOB) and whole cell patch clamp recordings were employed to study the intrinsic electrophysiological and synaptic properties of AOB mitral cells (MCs). The majority of MCs exhibited a spontaneous action potential firing rate that could be modulated by glutamate and GABA receptor antagonists. Excitatory and inhibitory spontaneous postsynaptic currents (psc's) were detected in the MCs, suggesting that inhibitory interneurons, in addition to vomeronasal organ (VNO) input, may influence MC output. As one AOB glomerulus can receive multiple VNO inputs, these results support the hypothesis that integration of pheromone signals may occur at the level of the AOB. The olfactory projection to the amygdala, and intra-amygdaloid projections, are limbic relays involved in behavioral reinforcement, a property that can be influenced by nicotine and mediated by presynaptic nicotinic acetylcholine receptors (nAChRs). Co-cultures consisting of murine olfactory bulb (OB) explants and dispersed amygdala neurons were developed to reconstruct this pathway in vitro. Patch-clamp recordings were obtained from amygdala neurons contacted by OB explant neurites, and spontaneous and evoked synaptic currents were characterized. The majority of innervated amygdala neurons exhibited glutamatergic spontaneous psc's and a smaller population exhibited GABAergic spontaneous psc's. Direct extracellular stimulation of OB explants elicited glutamatergic synaptic currents in amygdala neurons. Immunocytochemistry of the OB explants was consistent with the targeting of nAChR protein to presynaptic sites of MC projections. Hence, the role of presynaptic nAChRs in modulating synaptic transmission in these co-cultures was examined. Nicotine markedly increased the frequency of spontaneous psc's in 39% of neurons that exhibited glutamatergic spontaneous psc's and 35% of neurons that exhibited GABAergic spontaneous psc's (peak fold increase = 125.2 ± 33.3 and 63.9 ± 34.3, respectively). Thus, presynaptic nAChRs can enhance glutamatergic and GABAergic synaptic transmission in the amygdala, suggesting that they may modulate behaviors mediated by olfactory projections to the amygdala, where integration of olfactory and pheromonal input is thought to occur.
