Calcium in sympathetic boutons of rat superior cervical ganglion during facilitation, augmentation and potentiation.
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.
Lin
Y Q
YQ
Department of Physiology F13, University of Sydney, NSW, Australia.
Brain
K L
KL
Bennett
M R
MR
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
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