Nitric oxide stimulates glutamatergic synaptic inputs to baroreceptor neurons through potentiation of Cav2.2-mediated Ca(2+) currents.

Nitric oxide (NO) increases glutamate release to the second-order neurons in the nucleus tractus solitarius (NTS). N-type Ca(2+) channel is essential for triggering glutamate release at synaptic terminals. In this study, we determined the role of Cav2.2 subunit in NO-induced increase in glutamate synaptic inputs to NTS neurons. The second-order NTS neurons and nodose ganglionic (NG) neurons were identified by applying DiA, a fluorescent lipophilic tracer, on aortic depressor nerve in rats. NO donor DEA/NO significantly increased tractus solitarius (TS)-evoked excitatory postsynaptic currents (EPSCs) in second-order NTS neurons, an effect was abolished by pretreatment of slice with ODQ, an inhibitor for soluble isoform of guanylyl cyclase. DEA/NO decreased the paired-pulse ratio of TS-evoked EPSCs, while increased the frequency, but not the amplitude, of miniature EPSCs in second-order NTS neurons. Furthermore, DEA/NO significantly increased Ba(2+) currents in identified baroreceptor NG neurons. However, DEA/NO had little effect on the Ba(2+) currents in the presence of specific N-type Ca(2+) blocker ω-conotoxin GVIA. In addition, immunocytochemistry staining revealed that Cav2.2 subunit immunoreactivates were colocalized with DiA-labeled baroreceptor nerve terminals in the NTS. Collectively, these findings suggest that NO stimulates glutamatergic synaptic inputs to second-order NTS neurons through augmentation of Cav2.2-mediated N-type Ca(2+) currents.
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