title: Calcium in sympathetic boutons of rat superior cervical ganglion during facilitation, augmentation and potentiation.
abstract: The sympathetic preganglionic nerve terminals of the rat superior cervical ganglion were loaded with the calcium indicator oregon green 488 BAPTA-1 to measure the change in calcium concentration in the terminal boutons, (delta[Ca2+]b) following short (1 or 5 impulses) and long (200 impulses) trains at 30 Hz. The delta[Ca2+]b after a single action potential or a short train declined in two phases: a fast phase with a time constant of 530+/-30 ms and a moderate phase with a time constant of 4.0+/-0.2 s. The delta[Ca2+]b following a long train eventually declined with a time constant of 127+/-34 s (slow phase). The addition of either omega-agatoxin TK (100 nM), omega-conotoxin GVIA (100 nM) or nifedipine (20 microM) to block P-type, N-type or L-type calcium channels respectively showed that the rise in delta[Ca2+ ]b in boutons was predominantly mediated by an influx of calcium through P-type (53+/-7%) and N-type (46+/-4%) calcium channels. Experiments with caffeine, ryanodine and thapsigargin indicate that intracellular caffeine-sensitive calcium stores have a small but statistically significant effect on the fast and moderate phases. The mitochondrial uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP; 2 microM) significantly decreased the amplitude of the slow phase of delta[Ca2+]b relaxation, and sped its time course, suggesting that mitochondria normally dump calcium during this phase. Adenosine reduced the amplitude of delta[Ca2+]b in response to single action potentials by 30+/-6%, suggesting that adenosine-mediated autoinhibition in these boutons reduces Ca2+ influx. Spontaneous increases in delta[Ca2+]b demonstrated Ca2+ coupling between adjacent boutons. The delta[Ca2+]b kinetics are compared with F2 facilitation, augmentation and post-tetanic potentiation.
authors.affiliation: Department of Physiology F13, University of Sydney, NSW, Australia.
authors.forename: Y Q
authors.initials: YQ
authors.lastname: Lin
authors.forename: K L
authors.initials: KL
authors.lastname: Brain
authors.forename: M R
authors.initials: MR
authors.lastname: Bennett
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000241:Adenosine / Q000494:pharmacology; D000320:Adrenergic Fibers / Q000737:chemistry* / Q000502:physiology; D060848:Agatoxins; D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000032:analysis* / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone / Q000494:pharmacology; D000697:Central Nervous System Stimulants / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007476:Ionophores / Q000494:pharmacology; D007700:Kinetics; D009543:Nifedipine / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology; D017729:Presynaptic Terminals / Q000737:chemistry*; D051381:Rats; D017208:Rats, Wistar; D012433:Ryanodine / Q000494:pharmacology; D013111:Spider Venoms / Q000494:pharmacology; D017783:Superior Cervical Ganglion / Q000737:chemistry / Q000166:cytology*; D009435:Synaptic Transmission / Q000502:physiology*; D019284:Thapsigargin / Q000494:pharmacology; D020866:omega-Conotoxin GVIA
chemical_list: D060848:Agatoxins; D002121:Calcium Channel Blockers; D000697:Central Nervous System Stimulants; D002614:Chelating Agents; D004791:Enzyme Inhibitors; D007476:Ionophores; D010455:Peptides; D013111:Spider Venoms; C083855:omega-agatoxin-Aa4b; D012433:Ryanodine; D002110:Caffeine; D004533:Egtazic Acid; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone; D019284:Thapsigargin; D020866:omega-Conotoxin GVIA; D009543:Nifedipine; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D000241:Adenosine; D002118:Calcium