title: Nitric oxide stimulates glutamatergic synaptic inputs to baroreceptor neurons through potentiation of Cav2.2-mediated Ca(2+) currents.
abstract: 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.
authors.affiliation: Department of Critical Care, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA. Electronic address: dpli@mdanderson.org.
authors.forename: De-Pei
authors.initials: DP
authors.lastname: Li
authors.affiliation: Department of Anesthesiology and Perioperative Medicine, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.
authors.forename: Shao-Rui
authors.initials: SR
authors.lastname: Chen
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology*; D020864:Calcium Channels, N-Type / Q000502:physiology*; D019706:Excitatory Postsynaptic Potentials; D018698:Glutamic Acid / Q000378:metabolism*; D006834:Hydrazines / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D055369:Miniature Postsynaptic Potentials; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology*; D017207:Rats, Sprague-Dawley; D017552:Solitary Nucleus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D013569:Synapses / Q000502:physiology*
chemical_list: C503279:Cacna1b protein, rat; D020864:Calcium Channels, N-Type; D006834:Hydrazines; D020030:Nitric Oxide Donors; D009569:Nitric Oxide; D018698:Glutamic Acid; C084012:1,1-diethyl-2-hydroxy-2-nitrosohydrazine; D002118:Calcium
keywords: Baroreceptor; Brainstem; Ca(2+) channels; Glutamate; Nitric oxide