NGF attenuate angiotensin-induced facilitation of calcium channels in rat nucleus tractus solitarius

The nucleus tractus solitarius (NTS) is known to plays a major role in the regulation of cardiovascular, respiratory and gustatory functions. In addition, caudal NTS is believed to belong to the swallowing pattern generators, whereas the rostal NTS is part of the taste pathways. Neurotrophins, such as NGF and BDNF, promotes the development and neuronal survival mediated by activation of Trk receptor tyrosine kinases. Certain G-protein-coupled receptors (GPCRs) agonists have been shown to stimulate the tyrosine phosphorylation/trans-activation of growth factor receptors. It has been shown that activation of Trk receptor tyrosine kinases can interferes GPCRs mechanism. Voltage-dependent calcium channels (VDCCs) serve as crucial mediators of membrane excitability and calcium-dependent functions such as neurotransmitter release, enzyme activity and gene expression. We previously reported that Angiotensin 2 (Ang 2) and glutamate facilitate VDCCs mediated by GPCRs in NTS. Therefore, this study was designed to test the hypothesis that NGF and BDNF interferes with Ang 2- and glutamate-induced facilitation of VDCCs in NTS. Pretreatment with NGF and BDNF attenuated the Ang 2-induced facilitation of VDCCs but not glutamate-induced facilitation of VDCCs in NTS. NGF-induced attenuations were antagonized by pretreatment with TrkA receptor antagonist K-252a. These results indicated that NGF attenuated the Ang 2-induced facilitation of VDCCs mediated by TrkA receptor in NTS. [J Physiol Sci. 2008;58 Suppl:S131]