Potentiation of nicotinic receptor response by external calcium in rat central neurons.
Nicotinic acetylcholine receptor (nAChR) responses of rat medial habenular neurons are potentiated up to 3.5-fold by increasing the concentration of external Ca2+ in the millimolar range. This effect, independent of voltage, is probably due to the binding of Ca2+ to an external site. External Ca2+ decreases nAChR single-channel conductance at negative but not positive potentials, and it markedly enhances the frequency of opening of acetylcholine activated channels. The potentiating effect of Ca2+ is mimicked by Ba2+ and Sr2+, but barely by Mg2+. These data support the existence of positively acting allosteric sites for Ca2+, distinct from those involved in the decrease of single-channel conductance. A model in which external Ca2+ changes the properties of activation of the nAChR appears consistent with these data.
Mulle
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UA CNRS D1284, Département des Biotechnologies, Institut Pasteur, Paris, France.
Léna
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Changeux
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JP
D000495:Allosteric Site; D000818:Animals; D001464:Barium / Q000494:pharmacology; D001921:Brain / Q000187:drug effects / Q000502:physiology*; D002118:Calcium / Q000494:pharmacology*; D002413:Cations, Divalent; D004553:Electric Conductivity; D007700:Kinetics; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000502:physiology*; D013324:Strontium / Q000494:pharmacology
D002413:Cations, Divalent; D011978:Receptors, Nicotinic; D001464:Barium; D002118:Calcium; D013324:Strontium