title: Developmental changes in calcium current pharmacology and somatostatin inhibition in chick parasympathetic neurons.
abstract: Voltage-dependent calcium (Ca2+) currents were characterized and modulatory effects of somatostatin were measured in acutely dissociated chick ciliary ganglion neurons at embryonic stages 34, 37, and 40. This developmental time period coincides with the period of synapse formation between ciliary ganglion neurons and peripheral eye muscles. At all three developmental stages Ca2+ current could be blocked almost completely by combined application of omega-CgTX GVIA and nitrendipine. At young embryonic ages there was significant overlap in sensitivity, with approximately 75% of the current sensitive to either blocker applied independently. By stage 40, there was very little or no overlap in sensitivity, with approximately 75% of the current blocked by omega-CgTX GVIA (N-type) and 30% blocked by nitrendipine (L-type). These data are consistent with earlier findings that the pharmacology of acetylcholine release from ciliary ganglion nerve terminals changes during development from sensitivity to both dihydropyridines and omega-CgTX GVIA to selective sensitivity to omega-CgTX GVIA (Gray et al., 1992). Somatostatin reduced Ca2+ current by 50-60% at all three developmental stages. At early developmental stages somatostatin receptors coupled predominantly to the current that was sensitive to both omega-CgTX GVIA and nitrendipine. By stage 40, somatostatin primarily inhibited classically defined N-type current (selectively sensitive to omega-CgTX GVIA). Thus, somatostatin receptor coupling to Ca2+ channels persisted throughout development as Ca2+ current pharmacology changed.
authors.affiliation: Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA.
authors.forename: M G
authors.initials: MG
authors.lastname: White
authors.forename: M A
authors.initials: MA
authors.lastname: Crumling
authors.forename: S D
authors.initials: SD
authors.lastname: Meriney
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology*; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism; D002642:Chick Embryo; D002924:Ciliary Body / Q000166:cytology / Q000196:embryology; D005726:Ganglia, Parasympathetic / Q000166:cytology*; D006727:Hormone Antagonists / Q000494:pharmacology; D009474:Neurons / Q000737:chemistry / Q000166:cytology* / Q000187:drug effects; D009568:Nitrendipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D011758:Pyrroles / Q000494:pharmacology; D013004:Somatostatin / Q000494:pharmacology*; D013569:Synapses / Q000737:chemistry / Q000378:metabolism; D020866:omega-Conotoxin GVIA
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D006727:Hormone Antagonists; D010455:Peptides; D011758:Pyrroles; C071658:FPL 64176; D013004:Somatostatin; D020866:omega-Conotoxin GVIA; D009568:Nitrendipine; D002118:Calcium