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Differential Neurotrophic Regulation of Sodium and Calcium Channels in an Adult Sympathetic Neuron

Centre for Neuroscience and Department of Pharmacology, University of Alberta, Edmonton, Alberta, Canada

Submitted 27 August 2007; accepted in final form 19 January 2008

Adult neuronal phenotype is maintained, at least in part, by the sensitivity of individual neurons to a specific selection of neurotrophic factors and the availability of such factors in the neurons' environment. Nerve growth factor (NGF) increases the functional expression of Na⁺ channel currents (I_Na) and both N- and L-type Ca²⁺ currents (I_Ca,N and I_Ca,L) in adult bullfrog sympathetic ganglion (BFSG) B-neurons. The effects of NGF on I_Ca involve the mitogen-activated protein kinase (MAPK) pathway. Prolonged exposure to the ganglionic neurotransmitter luteinizing hormone releasing hormone (LHRH) also increases I_Ca,N but the transduction mechanism remains to be elucidated as does the transduction mechanism for NGF regulation of Na⁺ channels. We therefore exposed cultured BFSG B-neurons to chicken II LHRH (0.45 µM; 6–9 days) or to NGF (200 ng/ml; 9–10 days) and used whole cell recording, immunoblot analysis, and ras or rap-1 pulldown assays to study effects of various inhibitors and activators of transduction pathways. We found that 1) LHRH signals via ras-MAPK to increase I_Ca,N, 2) this effect is mediated via protein kinase C-β (PKC-β-II), 3) protein kinase A (PKA) is necessary but not sufficient to effect transduction, 4) NGF signals via phosphatidylinositol 3-kinase (PI3K) to increase I_Na, and 5) long-term exposure to LHRH fails to affect I_Na. Thus downstream signaling from LHRH has access to the ras-MAPK pathway but not to the PI3K pathway. This allows for differential retrograde and anterograde neurotrophic regulation of sodium and calcium channels in an adult sympathetic neuron.

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