Characterization of 5-HT-sensitive potassium conductances in neonatal rat facial motoneurones in vitro.
1. The properties of the 5-HT-sensitive K+ conductance of neonatal rat facial motoneurones were examined in brainstem slices using whole-cell patch-clamp techniques. 2. In a small proportion of motoneurones, 5-hydroxytryptamine (5-HT) evoked an inward current mediated solely by a decrease in K+ conductance. The reversal potential (V5-HT) was dependent on the external K+ concentration and the 5-HT-evoked current (I5-HT) displayed a linear current-voltage (I-V) relationship. 3. In the remaining motoneurones, the 5-HT-evoked decrease in K+ conductance could only be observed in isolation once a concomitant 5-HT-mediated enhancement of the hyperpolarization-activated current, Ih, had been abolished with the Ih blocker, ZD-7288. 4. External Cs+ also abolished the Ih-mediated component of I5-HT but, in addition, blocked part of the 5-HT-sensitive K+ current. At potentials hyperpolarized to V5-HT, Cs+ voltage dependently blocked I5-HT while at potentials depolarized to V5-HT, I5-HT was largely unaffected. Ba2+ and Rb+ had identical actions to Cs+ on the 5-HT-sensitive K+ current. 5. The Ba2+-, Rb+- and Cs+-sensitive component of the 5-HT-sensitive K+ current inwardly rectified with a reversal potential that was dependent on the K+ equilibrium potential (EK). 6. Replacing external Na+ with N-methyl-D-glucamine, blocking Ca2+ entry, or preventing an increase in intracellular [Ca2+] with BAPTA, all failed to alter I5-HT at potentials depolarized to EK. 7. I5-HT at depolarized potentials was reversibly blocked by 4-aminopyridine (4 mM) but not tetraethylammonium chloride (30 mM) and did not show inactivation during depolarizing voltage pulses (1.5 s duration). 8. The results suggest that, in addition to enhancing Ih, 5-HT modulates two distinct K+ conductances in neonatal rat facial motoneurones. The actions of Cs+, Ba2+ and Rb+ support the involvement of a member of the inwardly rectifying family of K+ channels while the other K+ channel may belong to the voltage-gated family.
Larkman
P M
PM
Department of Pharmacology, University of Edinburgh, 1 George Square, Edinburgh EH8 9JZ, UK. P.Larkman@ed.ac.uk
Kelly
J S
JS
D000818:Animals; D000831:Animals, Newborn; D001464:Barium / Q000494:pharmacology; D002586:Cesium / Q000494:pharmacology; D004553:Electric Conductivity; D005071:Evoked Potentials / Q000187:drug effects* / Q000502:physiology; D005154:Facial Nerve / Q000502:physiology*; D005260:Female; D066298:In Vitro Techniques; D007700:Kinetics; D008297:Male; D008536:Meglumine / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D011743:Pyrimidines / Q000494:pharmacology; D051381:Rats; D012413:Rubidium / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology*; D012964:Sodium / Q000494:pharmacology; D019789:Tetraethylammonium / Q000494:pharmacology
D015221:Potassium Channels; D011743:Pyrimidines; C082246:ICI D2788; D002586:Cesium; D001464:Barium; D012701:Serotonin; D019789:Tetraethylammonium; D008536:Meglumine; D012964:Sodium; D012413:Rubidium; D011188:Potassium