title: Potassium conductances underlying repolarization and after-hyperpolarization in rat CA1 hippocampal interneurones.
abstract: 1. The roles of multiple potassium conductances underlying action potential repolarization and after-hyperpolarization (AHP) in visually identified st. oriens-alveus (st. O-A) inhibitory interneurones of neonatal rat CA1 hippocampal slices were determined using whole-cell patch clamp techniques. 2. 4-Aminopyridine dose-dependently prolonged the action potential repolarization. The effects of 4-AP persisted in Ca(2+)-free conditions. Action potentials evoked from hyperpolarized potentials possessed an increased rate of repolarization. These data suggest an involvement of the rapidly activating transient current, IA, in spike repolarization. 3. Action potential duration was increased in the presence of Ca(2+)-free, Cd(2+)-containing solution, iberiotoxin or 1 mM TEA. The fast component of the AHP was attenuated by these agents suggesting that the Ca(2+)-activated K+ conductance, IC, underlies both the spike repolarization and fast AHP. 4. In Ca(2+)-free conditions, TEA (> 1 mM) dose-dependently prolonged the action potential duration by blocking a late conductance in action potential repolarization, suggesting a role for the sustained current, IK. 5. The slow AHP was attenuated by Ca(2+)-free medium, apamin or the Ca2+ chelator EGTA, suggesting a role for the Ca(2+)-activated K+ conductance, IAHP. 6. We conclude that action potential repolarization and AHP of st. O-A interneurones result from the activation of pharmacologically distinct, temporally overlapping potassium conductances. These findings are discussed with reference to the voltage clamp data presented in the preceding manuscript.
authors.affiliation: Laboratory of Cellular and Molecular Neurophysiology, NICHD-NIH, Bethesda, MD 20892-4495, USA.
authors.forename: L
authors.initials: L
authors.lastname: Zhang
authors.forename: C J
authors.initials: CJ
authors.lastname: McBain
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000200:Action Potentials / Q000502:physiology; D000588:Amines / Q000494:pharmacology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology; D002217:Carbachol / Q000494:pharmacology; D006624:Hippocampus / Q000166:cytology* / Q000502:physiology; D007395:Interneurons / Q000737:chemistry / Q000502:physiology*; D018721:Muscarinic Agonists / Q000494:pharmacology; D009433:Neural Inhibition / Q000502:physiology; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013997:Time Factors
chemical_list: D000588:Amines; D018721:Muscarinic Agonists; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D015124:8-Bromo Cyclic Adenosine Monophosphate; D001030:Apamin; D019789:Tetraethylammonium; D002217:Carbachol; D015761:4-Aminopyridine; D002118:Calcium