Transmitter release and calcium currents at an Aplysia buccal ganglion synapse--II. Modulation by presynaptic receptors.
Changes in evoked acetylcholine quantal release induced by histamine, FLRFamide and buccalin were investigated at an identified neuro-neuronal synapse in the buccal ganglion of Aplysia californica. Regulation of acetylcholine release by these neuromodulators was correlated with their actions on the presynaptic Ca2+ current. We have previously reported that FLRFamide and histamine, respectively, increase and decrease acetylcholine release from buccal neurons B4/B5. Buccalin, a peptide specific to the buccal ganglion, lowered the number of acetylcholine quanta released. Consistent with the synaptic effects, the presynaptic nifedipine-resistant Ca2+ current that triggers the release of acetylcholine in B4/B5 neurons [Trudeau L.-E. et al. (1993) Neuroscience 53, 571-580] was lowered by buccalin or by histamine and enhanced by FLRFamide. The analysis of tail currents showed that histamine shifts the voltage dependence of the nifedipine-resistant Ca2+ channels towards more positive voltages, whereas FLRFamide has an opposite action. Buccalin did not affect the voltage dependence of the channels but depressed the amplitude of the Ca2+ current, an effect which could be due either to a reduction of the number of available Ca2+ channels, to a decrease of their unitary conductance or to a modification of their gating. Inactivation of presynaptic G proteins prevented the modulatory actions of FLRFamide and histamine on quantal acetylcholine release and also on the voltage dependence of the nifedipine-resistant Ca2+ channels. This procedure, however, failed to prevent the suppressive effects of buccalin. The possibility of relating the voltage dependence shifts of the Ca2+ current induced by FLRFamide and histamine to the phosphorylation state of the Ca2+ channels is discussed. It is concluded that three independent presynaptic pathways initiated by histamine, FLRFamide and buccalin control presynaptic Ca2+ influx, these modulations being apparent within the physiological range of voltages required to activate Ca2+ channels.
Baux
G
G
Laboratoire de Neurobiologie Cellulaire et Moléculaire, C.N.R.S., Gif-sur-Yvette, France.
Fossier
P
P
Trudeau
L E
LE
Tauc
L
L
D000818:Animals; D001048:Aplysia / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D002927:Cimetidine / Q000494:pharmacology; D019204:GTP-Binding Proteins / Q000378:metabolism; D005724:Ganglia / Q000187:drug effects / Q000378:metabolism*; D006153:Guanosine Diphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D009479:Neuropeptides / Q000494:pharmacology; D018377:Neurotransmitter Agents / Q000378:metabolism*; D009543:Nifedipine / Q000494:pharmacology; D009842:Oligopeptides / Q000494:pharmacology; D010275:Parasympathetic Nervous System / Q000187:drug effects / Q000378:metabolism; D013569:Synapses / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000502:physiology; D013873:Thionucleotides / Q000494:pharmacology
D015220:Calcium Channels; D009479:Neuropeptides; D018377:Neurotransmitter Agents; D009842:Oligopeptides; D013873:Thionucleotides; C058692:buccalin; D006153:Guanosine Diphosphate; C023427:guanosine 5'-O-(2-thiodiphosphate); D002927:Cimetidine; C066148:phenylalanyl-leucyl-arginyl phenylalaninamide; D006632:Histamine; D019204:GTP-Binding Proteins; D009543:Nifedipine