Social discrimination in rats relies on vasopressin cells (VPCs), neurons intrinsic to the olfactory bulb (OB). We previously observed that VPCs responded to electrical stimulation of the olfactory nerve in acute OB slices with inhibitory postsynaptic potentials (IPSPs), and that the neuromodulator acetylcholine (ACh) was able to switch these responses to excitation, often resulting in action potentials (AP). Moreover, in behaving rats exposed to conspecifics, more VPCs were immunopositive to the neural activity marker pERK (pERK+ VPC) than in control rats. Is this increased ERK activation indeed related to cholinergic modulation?
Here we investigated ERK activation in acute OB slices from transgenic VP-eGFP rats upon various treatments. Both KCl and NMDA stimulation resulted in substantial pERK induction across bulbar neurons including mitral cells and caused VPC spiking, but neither increased pERK+ VPC percentage. Conversely, TTX treatment further reduced VPC ERK activation compared to control, indicating spontaneous activity of VPCs, which we also observed in a subset of VPCs in electrophysiological recordings. Tetanic olfactory nerve stimulation yielded regionalized, column-like ERK activation across bulbar layers. While ACh alone had no influence on pERK induction in VPCs, the presence of ACh during tetanic stimulation substantially increased percentages of pERK+ VPCs specifically within activated regions, implying that coincident cholinergic neuromodulation and afferent synaptic inputs cooperate to induce pERK in VPCs.
While depolarization alone is insufficient to trigger the pERK induction cascade in VPCs, our results thus validate pERK induction as a tool to monitor synaptic, suprathreshold VPC excitation in the OB.