Voltage-dependent Ca2+ influx into identified leech neurones.
We determined the relationships between the intracellular free Ca2+ concentration ([Ca2+]i) and the membrane potential (Em) of six different neurones in the leech central nervous system: Retzius, 50 (Leydig), AP, AE, P, and N neurones. The [Ca2+]i was monitored by using iontophoretically injected fura-2. The membrane depolarization evoked by raising the extracellular K+ concentration ([K+]o) up to 89 mM caused a persistent increase in [Ca2+]i, which was abolished in Ca(2+)-free solution indicating that it was due to Ca2+ influx. The threshold membrane potential that must be reached in the different types of neurones to induce a [Ca2+]i increase ranged between -40 and -25 mV. The different threshold potentials as well as differences in the relationships between [Ca2+]i and EM were partly due to the cell-specific generation of action potentials. In Na(+)-free solution, the action potentials were suppressed and the [Ca2+]i/Em relationships were similar. The K(+)-induced [Ca2+]i increase was inhibited by the polyvalent cations Co2+, Ni2+, Mn2+, Cd2+, and La3+, as well as by the cyclic alcohol menthol. Neither the polyvalent cations nor menthol had a significant effect on the K(+)-induced membrane depolarization. Our results suggest that different leech neurones possess voltage-dependent Ca2+ channels with similar properties.
Dierkes
P W
PW
Institut für Neurobiologie, Heinrich-Heine-Universität Düsseldorf, Germany.
Hochstrate
P
P
Schlue
W R
WR
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D000982:Antipruritics / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D003035:Cobalt / Q000494:pharmacology; D004594:Electrophysiology; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology*; D007811:Lanthanum / Q000494:pharmacology; D007865:Leeches / Q000502:physiology*; D008610:Menthol / Q000494:pharmacology; D009046:Motor Neurons / Q000737:chemistry* / Q000187:drug effects / Q000502:physiology; D009532:Nickel / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism
D000982:Antipruritics; D015220:Calcium Channels; D015221:Potassium Channels; D008610:Menthol; D003035:Cobalt; D007811:Lanthanum; D009532:Nickel; D011188:Potassium; D002118:Calcium