HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 95/1/196    most recent 00630.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Wilson, C. J. Articles by Goldberg, J. A. Search for Related Content PubMed PubMed Citation Articles by Wilson, C. J. Articles by Goldberg, J. A.

Origin of the Slow Afterhyperpolarization and Slow Rhythmic Bursting in Striatal Cholinergic Interneurons

Department of Biology, University of Texas, San Antonio, Texas

Submitted 16 June 2005; accepted in final form 12 September 2005

Striatal cholinergic interneurons recorded in slices exhibit three different firing patterns: rhythmic single spiking, irregular bursting, and rhythmic bursting. The rhythmic single-spiking pattern is governed mainly by a prominent brief afterhyperpolarization (mAHP) that follows single spikes. The mAHP arises from an apamin-sensitive calcium-dependent potassium current. A slower AHP (sAHP), also present in these neurons, becomes prominent during rhythmic bursting or driven firing. Although not apamin sensitive, the sAHP is caused by a calcium-dependent potassium conductance. It is not present after blockade of calcium current with cadmium or after calcium is removed from the media or when intracellular calcium is buffered with bis-(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid. It reverses at the potassium equilibrium potential. It can be generated by subthreshold depolarizations and persists after blockade of sodium currents by tetrodotoxin. It is slow, being maximal 1 s after depolarization onset, and takes several seconds to decay. It requires >300-ms depolarizations to become maximally activated. Its voltage sensitivity is sigmoidal, with a half activation voltage of –40 mV. We conclude the sAHP is a high-affinity apamin-insensitive calcium-dependent potassium conductance, triggered by calcium currents partly activated at subthreshold levels. In combination with those calcium currents, it accounts for the slow oscillations seen in a subset of cholinergic interneurons exhibiting rhythmic bursting. In all cholinergic interneurons, it contributes to the slowdown or pause in firing that follows driven activity or prolonged subthreshold depolarizations and is therefore a candidate mechanism for the pause response observed in cholinergic neurons in vivo.

This article has been cited by other articles:

				J. A. Goldberg, M. A. Teagarden, R. C. Foehring, and C. J. Wilson Nonequilibrium Calcium Dynamics Regulate the Autonomous Firing Pattern of Rat Striatal Cholinergic Interneurons J. Neurosci., July 1, 2009; 29(26): 8396 - 8407. [Abstract] [Full Text] [PDF]

				C. O. Tan and D. Bullock A Dopamine-Acetylcholine Cascade: Simulating Learned and Lesion-Induced Behavior of Striatal Cholinergic Interneurons J Neurophysiol, October 1, 2008; 100(4): 2409 - 2421. [Abstract] [Full Text] [PDF]

				E. Hong, F. Gurel Kazanci, and A. A. Prinz Different Roles of Related Currents in Fast and Slow Spiking of Model Neurons From Two Phyla J Neurophysiol, October 1, 2008; 100(4): 2048 - 2061. [Abstract] [Full Text] [PDF]

				P. Deng, Y. Zhang, and Z. C. Xu Involvement of Ih in Dopamine Modulation of Tonic Firing in Striatal Cholinergic Interneurons J. Neurosci., March 21, 2007; 27(12): 3148 - 3156. [Abstract] [Full Text] [PDF]