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The Journal of Neuroscience, August 6, 2003, 23(18):7169-7175

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Neurotrophic Regulation of Calcium Channels by the Peptide Neurotransmitter Luteinizing Hormone Releasing Hormone

Christopher P. Ford,² William F. Dryden,^1,2 and Peter A. Smith^1,2

¹Department of Pharmacology and ²Center for Neuroscience, University of Alberta, Edmonton, Alberta, Canada T6G 2H7

We exploited the simple organization of bullfrog paravertebral sympathetic ganglia (BFSG) to test whether the neurotransmitter peptide luteinizing hormone releasing hormone (LHRH), which generates the late slow EPSP, could also exert long-term neurotrophic control of ion channel expression. Whole-cell recordings from B-cells in BFSG showed that removal of all of the sources of ganglionic LHRH for 10 d by cutting preganglionic C-fibers in vivo caused a 28% reduction in Ca²⁺ current density. When BFSG B-neurons were dissociated from adult bullfrogs and maintained in a defined-medium, neuron-enriched, low-density, serum-free culture, the I_Ca density was increased by 49% after 6-7 d in the presence of 0.45 µM LHRH. This increase was not associated with alterations in the voltage dependence of Ca²⁺ current activation or inactivation and reflected a selective increase in N-type Ca²⁺ channel current. The increase in I_Ca density induced by LHRH was blocked by the transcription inhibitor actinomycin D. These results suggest that chronic exposure to a neurotransmitter that acts through G-protein-coupled receptors exerts long-term control of ion channel expression in a fully differentiated, adult sympathetic neuron in vitro or in vivo.

Key words: gonadotropin hormone releasing hormone; Ras; MAP kinase; protein kinase C; sympathetic; autonomic; G-protein-coupled receptor; GPCR; G_q

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Received Apr. 24, 2003; revised Jun. 10, 2003; accepted Jun. 11, 2003.

This article has been cited by other articles:

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