title: Bursting activity in leech Retzius neurons induced by low external chloride.
abstract: We have investigated the bursting activity of Retzius neurons in the central nervous system of the leech Hirudo medicinalis as induced in Cl(-)-free saline by measuring membrane potential, membrane current and the intracellular calcium concentration ([Ca2+]i), using fura-2 or Oregon-Green488-Bapta-1. The Retzius neurons changed their low tonic firing to rhythmical bursting activity when the extracellular Cl- concentration ([Cl-]o) was lowered to 1 mM or less. In Cl(-)-free saline (Cl- exchanged by gluconate), bursting was accompanied by a rise in intracellular Ca2+ in both cell body and axon, which oscillated in synchrony with the bursts. The Ca2+ transients depended on the amplitude and duration of the depolarization underlying the burst, and were presumably due to Ca2+ influx through voltage-dependent Ca2+ channels. In Ca(2+)-free, EGTA-buffered saline or in the presence of Ca2+ channel blockers verapamil (1 mM) or diltiazem (500 microM) the depolarizations underlying the bursts in Cl(-)-free saline were enhanced in amplitude and duration. Bursting was not affected by depleting the intracellular Ca2+ stores with cyclopiazonic acid. The depolarization in Cl(-)- and Ca(2+)-free saline did not evoke intracellular Ca2+ changes. The burst-underlying membrane depolarization induced by Cl- removal was found to be due to a Na(+)-dependent persistent inward current and could be inhibited by saxitoxin (25-50 microM). The results suggest that a persistent Na+ current is generated in Cl(-)-free saline and induces the depolarization underlying rhythmic activity, and that presumably Ca(2+)-induced K+ currents modulate the bursting behaviour.
authors: Abteilung für Allgemeine Zoologie, FB Biologie, Universität Kaiserslautern, Postfach 3049, 67653 Kaiserslautern, Germany. abeck@rhrk.uni-kl.de
authors: A
authors: A
authors: Beck
authors: C
authors: C
authors: Lohr
authors: W
authors: W
authors: Nett
authors: J W
authors: JW
authors: Deitmer
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002712:Chlorides / Q000008:administration & dosage* / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004553:Electric Conductivity; D004594:Electrophysiology; D007425:Intracellular Membranes / Q000378:metabolism; D007865:Leeches / Q000502:physiology*; D009474:Neurons / Q000187:drug effects* / Q000502:physiology*; D012964:Sodium / Q000494:pharmacology / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology
chemical_list: D002121:Calcium Channel Blockers; D002712:Chlorides; D012964:Sodium; D002118:Calcium