Brain-derived Neurotrophic Factor in Autonomic Nervous System: Nicotinic Acetylcholine Receptor Regulation and Potential Trophic Effects

by Zhou, Xiangdong

Abstract (Summary)
Neurotrophin family is composed of several neurotrophin molecules. BDNF, as one of the widely studied family members, is a potent molecule in promoting the neuronal survival and regulating synaptic functions demonstrated in a variety of systems. However, in the chicken CG neurons, general wisdom considers the irrelevance of BDNF to this classic model of the parasympathetic system. In this study, both the expression and the potential function of BDNF/TrkB in the chicken CG were carefully investigated. BDNF, as well as its functional receptor TrkB, were both detected in the CG neurons during the embryonic stage (E8-E14). Application of BDNF in the culture specifically upregulated the surface binding sites and the transcript level of a7 nAChRs, but not those of a3*-nAChRs. The full length TrkB receptor was shown essential for the BDNF induced regulation. In addition, whole-cell currents mediated by a7 nAChRs and synaptic activities dramatically increased following the same treatment. Interestingly, BDNF was shown as a survival-promoting neurotrophic factor in vitro as well. The BDNF expression and release in culture was upregulated by the depolarization. Moreover, depolarization-induced survival of CG neurons was attenuated with the application of BDNF antibody which blocks the endogenous BDNF function. Combined with the fact that an increase was detected in the level of released BDNF in the culture media, such results above imply the potential BDNF autocrine pathway in promoting activity-dependent CG neuronal survival. Based on the expression pattern of BDNF during the embryogenesis, it is quite reasonable to speculate that BDNF may support CG neuronal survival and regulate receptor expression, function and synaptic activity in vivo.
Bibliographical Information:


School:University of Toledo Health Science Campus

School Location:USA - Ohio

Source Type:Master's Thesis

Keywords:brain derived neurotrophic factor ciliary ganglion nicotinic acetylcholine receptor neurotrophin


Date of Publication:01/01/2005

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