Calcium-dependent potassium conductance in guinea-pig olfactory cortex neurones in vitro.
1. Guinea-pig olfactory cortex neurones in vitro (23-25 degrees C) were voltage clamped by means of a single-micro-electrode sample-and-hold technique. 2. Under current clamp at the resting potential (approximately -80 mV), brief depolarizing stimuli evoked trains of action potentials with little visible after-potential. However, in 90% of recorded cells held at membrane potentials between -70 and -45 mV, depolarizing current pulses evoked a slow after-hyperpolarization (a.h.p.) (approximately 8 mV) lasting several seconds and accompanied by an increase in input conductance. 3. The outward membrane current underlying the a.h.p. was revealed either by switching rapidly to voltage clamp at the end of a spike train ('hybrid' clamp) or by applying brief depolarizing commands from potentials between -60 to -45 mV. The tail current showed a distinct rising phase (time to peak approximately 1 s) and exponential decay (tau approximately 3 s) and was suppressed by removal of external Ca2+, or adding Co2+ (1-2 mM), Cd2+ (200 microM) or Mg2+ (6 mM). The a.h.p. current reversal potential was -96 mV in 3 mM-K+ medium. 4. Low concentrations (1-2 microM) of muscarine, carbachol, oxotremorine or the muscarinic ganglion stimulant, McN-A-343 (1-10 microM) reduced the a.h.p. current and leak conductance and induced a steady inward current, without affecting M-current (IM) relaxations. IM inhibition generally required higher (greater than 10 microM) agonist concentrations, although oxotremorine remained ineffective at up to 50 microM. 5. The a.h.p. current was reduced by noradrenaline and tetraethylammonium (TEA), but not by apamin or tubocurarine. Apart from TEA, these agents had no effect on IM. 6. Addition of tetrodotoxin (TTX, 1 microM) or removing external Na+ depressed the a.h.p. current amplitude recorded under voltage clamp. The residual tail current could be further reduced by adding Cd2+ or muscarinic agonists. 7. Repolarizing tail currents induced following positive voltage commands consisted mainly of IM and slow a.h.p. current with little evidence of a 'fast' Ca2+-activated K+ current (IC). 8. It is concluded that the slow a.h.p. current that underlies the post-burst after-hyperpolarization of olfactory neurones, is a Ca2+-dependent K+ current distinct from IM. It is suggested that the cholinergic modulation of this current (rather than IM) may provide a more subtle control of cell excitability in cortical neurones.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002413:Cations, Divalent / Q000494:pharmacology; D002540:Cerebral Cortex / Q000502:physiology*; D005260:Female; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D008297:Male; D009474:Neurons / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D010277:Parasympathomimetics / Q000494:pharmacology; D011188:Potassium / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
D002413:Cations, Divalent; D007473:Ion Channels; D010277:Parasympathomimetics; D013757:Tetraethylammonium Compounds; D013779:Tetrodotoxin; D019789:Tetraethylammonium; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine