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The Journal of Neuroscience, May 5, 2004, 24(18):4340-4350; doi:10.1523/JNEUROSCI.0055-04.2004

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Cellular/Molecular
Brain-Derived Neurotrophic Factor and trkB Signaling in Parasympathetic Neurons: Relevance to Regulating 7-Containing Nicotinic Receptors and Synaptic Function

Xiangdong Zhou, Qiang Nai, ^* Min Chen, ^* Jason D. Dittus, Marthe J. Howard, and Joseph F. Margiotta

Medical College of Ohio, Department of Anatomy and Neurobiology, Toledo, Ohio 43614-5804

Parasympathetic neurons do not require neurotrophins for survival and are thought to lack high-affinity neurotrophin receptors (i.e., trks). We report here, however, that mRNAs encoding both brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tropomyosin-related kinase B (trkB) are expressed in the parasympathetic chick ciliary ganglion (CG) and that BDNF-like protein is present in the ganglion and in the iris, an important peripheral target of ciliary neurons. Moreover, CG neurons express surface trkB and exogenous BDNF not only initiates trk-dependent signaling, but also alters nicotinic acetylcholine receptor (nAChR) expression and synaptic transmission. In particular, BDNF applied to CG neurons rapidly activates cAMP-dependent response element-binding protein (CREB), and over the long-term selectively upregulates expression of 7-subunit-containing, homomeric nAChRs (7-nAChRs), increasing 7-subunit mRNA levels, 7-nAChR surface sites, and 7-nAChR-mediated whole-cell currents. At nicotinic synapses formed on CG neurons in culture, brief and long-term BDNF treatments also increase the frequency of spontaneous EPSCs, most of which are mediated by heteromeric nAChRs containing 3, 5, 4, and 2 subunits (3*-nAChRs) with a minor contribution from 7-nAChRs. Our findings demonstrate unexpected roles for BDNF-induced, trk-dependent signaling in CG neurons, both in regulating expression of 7-nAChRs and in enhancing transmission at 3*-nAChR-mediated synapses. The presence of BDNF-like protein in CG and iris target coupled with that of functional trkB on CG neurons raise the possibility that signals generated by endogenous BDNF similarly influence 7-nAChRs and nicotinic synapses in vivo.

Key words: ciliary ganglion; nicotinic acetylcholine receptor; BDNF; trkB; patch-clamp; neurotrophin; bungarotoxin; EPSC; cAMP response element-binding protein (CREB); PACAP

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Received Jan 7, 2004; revised March 9, 2004; accepted March 11, 2004.

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