Suppression of potassium channels elicits calcium-dependent plateau potentials in suprachiasmatic neurons of the rat.
By using whole-cell recordings in acute and organotypic hypothalamic slices, we found that following K+ channel blockade, sustained plateau potentials can be elicited by current injection in suprachiasmatic neurons. In an attempt to determine the ionic basis of these potentials, ion-substitution experiments were carried out. It appeared that to generate plateau potentials, calcium influx was required. Plateau potentials were also present when extracellular calcium was replaced by barium, but were independent upon an increase in the intracellular free calcium concentration. Substitution of extracellular sodium by the impermeant cation N-methyl-D-glucamine indicated that sodium influx could also contribute to plateau potentials. To gain some information on the pharmacological profile of the Ca++ channels responsible for plateau potentials, selective blocker of various types of Ca++ channel were tested. Plateau potentials were unaffected by isradipine, an L-type Ca++ channel blocker. However, they were slightly reduced by omega-conotoxin GVIA and omega-agatoxin TK, blockers of N-type and P/Q-type Ca++ channels, respectively. These data suggest that R-type Ca++ channels probably play a major role in the genesis of plateau potentials. We speculate that neurotransmitters/neuromodulators capable of reducing or suppressing potassium conductance(s) may elicit a Ca++-dependent plateau potential in suprachiasmatic neurons, thus promoting sustained firing activity and neuropeptide release.
Pierson
Patricia M
PM
Laboratoire de Physiologie Cellulaire et Moléculaire, CNRS UMR 6548, Faculté des Sciences, Université de Nice-Sophia Antipolis, 06108 Nice Cedex 2, France.
Liu
Xinhuai
X
Raggenbass
Mario
M
D000818:Animals; D001464:Barium / Q000378:metabolism / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D020908:Calcium Channels, R-Type / Q000187:drug effects / Q000502:physiology; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D002614:Chelating Agents / Q000494:pharmacology; D004558:Electric Stimulation; D045604:Extracellular Fluid / Q000378:metabolism; D008274:Magnesium / Q000378:metabolism / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D009924:Organ Culture Techniques; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology; D013493:Suprachiasmatic Nucleus / Q000187:drug effects / Q000378:metabolism*
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D020908:Calcium Channels, R-Type; D002614:Chelating Agents; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D001464:Barium; D012964:Sodium; D008274:Magnesium; D002118:Calcium