title: Neurotrophic regulation of calcium channels by the peptide neurotransmitter luteinizing hormone releasing hormone.
abstract: 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 ICa density was increased by 49% after 6-7 d in the presence of 0.45 microm 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 ICa 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.
authors.affiliation: Department of Pharmacology and Center for Neuroscience, University of Alberta, Edmonton, Alberta, Canada T6G 2H7.
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Ford
authors.forename: William F
authors.initials: WF
authors.lastname: Dryden
authors.forename: Peter A
authors.initials: PA
authors.lastname: Smith
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000378:metabolism; D020864:Calcium Channels, N-Type / Q000187:drug effects / Q000378:metabolism; D002478:Cells, Cultured; D003714:Denervation; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D005728:Ganglia, Sympathetic / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D015870:Gene Expression / Q000187:drug effects / Q000502:physiology; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology / Q000502:physiology*; D009413:Nerve Fibers, Myelinated / Q000502:physiology; D036421:Nerve Fibers, Unmyelinated / Q000502:physiology; D009414:Nerve Growth Factors / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000494:pharmacology / Q000502:physiology*; D018408:Patch-Clamp Techniques; D011892:Rana catesbeiana; D011966:Receptors, LHRH / Q000378:metabolism; D013997:Time Factors
chemical_list: D015220:Calcium Channels; D020746:Calcium Channels, L-Type; D020864:Calcium Channels, N-Type; D009414:Nerve Growth Factors; D018377:Neurotransmitter Agents; D011966:Receptors, LHRH; D007987:Gonadotropin-Releasing Hormone; D002118:Calcium