title: Contractions of the squid stellate ganglion.
abstract: Optical recording methods were used to characterize the intrinsic movements of squid stellate ganglia. Ganglionic contractions were rhythmic and occurred at a mean frequency of 8 min-1. Contractions were eliminated when Na+ in the external saline were replaced by Tris, but were only slowed when Na+ was replaced by sucrose. This suggests that Na+ plays some role in generating the contractions, but the complete abolition produced by Tris-containing saline may be due to a secondary pharmacological action of this ion. The Na+ channel blocker, tetrodotoxin, had no effect on contractions. Contractions were eliminated by removal of external Ca2+, by treatment with the inorganic Ca2+ channel blockers Mn2+ and Cd2+, or by treatment with the organic dihydropyridine Ca2+ channel blockers nitrendipine and nimodipine. Thus, extracellular Ca2+ plays an important role in generating the contractions. Because dihydropyridines eliminate contractions, but not synaptic transmission, they offer a means of studying transmission at the giant synapse of the stellate ganglion without having to contend with ganglionic movement. Electron microscopy of stellate ganglia revealed the presence of two types of cell that contained the organized arrays of cytoskeletal elements usually associated with contractile cells. One type was a pericyte that surrounded blood vessels within the stellate ganglion. The second type was distributed throughout the ganglion and resembled a smooth muscle cell. Either of these cell types might generate ganglionic contractions.
authors.affiliation: Department of Biological Sciences, University of Southern California, Los Angeles 90089-2520.
authors.forename: M E
authors.initials: ME
authors.lastname: Sanchez
authors.forename: C M
authors.initials: CM
authors.lastname: Nuño
authors.forename: J
authors.initials: J
authors.lastname: Buchanan
authors.forename: G J
authors.initials: GJ
authors.lastname: Augustine
mesh_terms: D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D003599:Cytoskeleton / Q000648:ultrastructure; D049832:Decapodiformes / Q000502:physiology*; D005728:Ganglia, Sympathetic / Q000502:physiology* / Q000648:ultrastructure; D008345:Manganese / Q000494:pharmacology; D008854:Microscopy, Electron; D009068:Movement / Q000187:drug effects / Q000502:physiology; D009553:Nimodipine / Q000494:pharmacology; D009568:Nitrendipine / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology / Q000502:physiology; D013569:Synapses / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002104:Cadmium; D008345:Manganese; D013779:Tetrodotoxin; D009553:Nimodipine; D009568:Nitrendipine; D012964:Sodium; D002118:Calcium