Nitric oxide stimulates glutamatergic synaptic inputs to baroreceptor neurons through potentiation of Cav2.2-mediated Ca(2+) currents.
Nitric oxide stimulates glutamatergic synaptic inputs to baroreceptor neurons through potentiation of Cav2.2-mediated Ca(2+) currents.
复制标题
一氧化氮通过增强 Cav2.2 介导的 Ca(2 ) 电流来刺激压力感受器神经元的谷氨酸突触输入。
DOI：
10.1016/j.neulet.2014.03.036
复制
发表时间：
2014
影响因子：
2.5
通讯作者：
Chen,Shao-Rui
中科院分区：
文献类型：
--
作者：
Li,De-Pei;Chen,Shao-Rui
Nitric oxide (NO) increases glutamate release to the second-order neurons in the nucleus tractus solitarius (NTS). N-type Ca2+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 Ba2+currents in identified baroreceptor NG neurons. However, DEA/NO had little effect on the Ba2+currents in the presence of specific N-type Ca2+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 Ca2+currents.
