PMID- 15342739 OWN - NLM STAT- MEDLINE DCOM- 20050405 LR - 20200225 IS - 1529-2401 (Electronic) IS - 0270-6474 (Print) IS - 0270-6474 (Linking) VI - 24 IP - 35 DP - 2004 Sep 1 TI - Muscarinic receptor modulation of slow afterhyperpolarization and phasic firing in rat supraoptic nucleus neurons. PG - 7718-26 AB - A slow posttrain afterhyperpolarization (sAHP) was studied in rat magnocellular neurosecretory cells (MNCs) in vitro. The sAHP was isolated from other afterpotentials by blocking the depolarizing afterpotential (DAP) with Cs(+) and the medium afterhyperpolarization (mAHP) with apamin. The sAHP amplitude increased logarithmically with activity ( approximately 3 mV per e-fold increase in number of impulses) and, when firing stopped, decayed exponentially with a time constant of 2 sec. The sAHP was associated with increased membrane conductance, and its amplitude varied linearly with voltage, reversing at the K(+) equilibrium potential. The sAHP was blocked by Cd(2+) but not by charybdotoxin or iberiotoxin, blockers of intermediate- and big-conductance-type Ca(2+)-dependent K(+) (K(Ca)) channels. The sAHP was reversibly inhibited by muscarine, an effect antagonized by atropine, indicating involvement of muscarinic cholinergic receptors. Muscarine did not affect Ca(2+)-dependent features of action potentials, DAPs, or the mAHP in MNCs, indicating selective modulation of K(Ca) channels causing the sAHP. Muscarinic inhibition of the sAHP enhanced plateau potentials and increased the mean firing rate and duration of afterdischarges that followed spike trains evoked from voltages near threshold. Similarly, the frequency and duration of the spontaneous phasic bursts that characterize physiologically activated vasopressin-releasing MNCs were enhanced by muscarine. MNCs thus express apamin- and voltage-insensitive K(Ca) channels that mediate an sAHP. The activity dependence and kinetics of the sAHP cause it to mask DAPs in a manner that attenuates the amplitude of plateau potentials. Muscarinic inhibition of the sAHP provides an effective mechanism for promoting phasic firing in MNCs. FAU - Ghamari-Langroudi, Masoud AU - Ghamari-Langroudi M AD - Centre for Research in Neuroscience, Montreal General Hospital and McGill University, Montreal, Quebec H3G 1A4, Canada. FAU - Bourque, Charles W AU - Bourque CW LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - J Neurosci JT - The Journal of neuroscience : the official journal of the Society for Neuroscience JID - 8102140 RN - 0 (Ion Channels) RN - 0 (Peptides) RN - 0 (Receptors, Muscarinic) RN - 00BH33GNGH (Cadmium) RN - 11000-17-2 (Vasopressins) RN - 115422-61-2 (Charybdotoxin) RN - 24345-16-2 (Apamin) RN - 4368-28-9 (Tetrodotoxin) RN - 773HER9B6T (iberiotoxin) RN - 7C0697DR9I (Atropine) RN - 7T101UWZ5W (Muscarine) RN - RWP5GA015D (Potassium) RN - SY7Q814VUP (Calcium) SB - IM MH - Action Potentials/drug effects MH - Animals MH - Apamin/pharmacology MH - Atropine/pharmacology MH - Cadmium/pharmacology MH - Calcium/metabolism/pharmacology MH - Cells, Cultured/drug effects/physiology MH - Charybdotoxin/pharmacology MH - Ion Channels/physiology MH - Ion Transport MH - Male MH - Membrane Potentials MH - Muscarine/pharmacology MH - Neurons/drug effects/*physiology MH - Organ Culture Techniques MH - Peptides/pharmacology MH - Potassium/metabolism MH - Rats MH - Rats, Long-Evans MH - Receptors, Muscarinic/*physiology MH - Supraoptic Nucleus/*cytology MH - Tetrodotoxin/pharmacology MH - Vasopressins/metabolism PMC - PMC6729628 EDAT- 2004/09/03 05:00 MHDA- 2005/04/06 09:00 PMCR- 2005/03/01 CRDT- 2004/09/03 05:00 PHST- 2004/09/03 05:00 [pubmed] PHST- 2005/04/06 09:00 [medline] PHST- 2004/09/03 05:00 [entrez] PHST- 2005/03/01 00:00 [pmc-release] AID - 24/35/7718 [pii] AID - 10.1523/JNEUROSCI.1240-04.2004 [doi] PST - ppublish SO - J Neurosci. 2004 Sep 1;24(35):7718-26. doi: 10.1523/JNEUROSCI.1240-04.2004.