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: 95/4/2352    most recent 00525.2005v1 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 (3) Citing Articles via Google Scholar Google Scholar Articles by Gillies, A. Articles by Willshaw, D. Search for Related Content PubMed PubMed Citation Articles by Gillies, A. Articles by Willshaw, D.

Membrane Channel Interactions Underlying Rat Subthalamic Projection Neuron Rhythmic and Bursting Activity

Institute for Adaptive and Neural Computation, School of Informatics, University of Edinburgh, Edinburgh, United Kingdom

Submitted 20 May 2005; accepted in final form 1 September 2005

A computational model of the rat subthalamic nucleus projection neuron is constructed using electrophysiological and morphological data and a restricted set of channel specifications. The model cell exhibits a wide range of electrophysiological behaviors characteristic of rat subthalamic neurons. It reveals that a key set of three channels play a primary role in distinguishing behaviors: a high-voltage-activated calcium channel (Ca_v1.2.-1.3), a low-voltage-activated calcium channel (Ca_v3.-), and a small current calcium-activated potassium channel (K_Ca2.1–2.3). Short and long posthyperpolarization rebound responses, low-frequency rhythmic bursting (<1 Hz), higher-frequency rhythmic bursting (4–7 Hz), and slow action and depolarizing potentials are behaviors all mediated by the interaction of these channels. This interaction can generate a robust calcium-dependent extended depolarization in the dendrites (a depolarizing plateau). The diversity observed in the rat subthalamic physiology (such as short or long rebounds, or the presence of low-frequency rhythmic busting) can arise from alterations in both the density and distributions of these channel types and, consequently, their ability to generate this depolarizing plateau. A number of important predictions arise from the model. For example, blocking or disrupting the low-voltage-activated Ca_v3.- calcium current should mute the emergence of rebound responses and rhythmic bursting. Conversely, increasing this channel current via large hyperpolarizing potentials in combination with partial blockade of the high-voltage-activated calcium channels should lead to the more experimentally elusive in vitro high-frequency bursting.

This article has been cited by other articles:

				M. D. Johnson and C. C. McIntyre Quantifying the Neural Elements Activated and Inhibited by Globus Pallidus Deep Brain Stimulation J Neurophysiol, November 1, 2008; 100(5): 2549 - 2563. [Abstract] [Full Text] [PDF]

				S. Ramanathan, T. Tkatch, J. F. Atherton, C. J. Wilson, and M. D. Bevan D2-Like Dopamine Receptors Modulate SKCa Channel Function in Subthalamic Nucleus Neurons Through Inhibition of Cav2.2 Channels J Neurophysiol, February 1, 2008; 99(2): 442 - 459. [Abstract] [Full Text] [PDF]

				S. Miocinovic, M. Parent, C. R. Butson, P. J. Hahn, G. S. Russo, J. L. Vitek, and C. C. McIntyre Computational Analysis of Subthalamic Nucleus and Lenticular Fasciculus Activation During Therapeutic Deep Brain Stimulation J Neurophysiol, September 1, 2006; 96(3): 1569 - 1580. [Abstract] [Full Text] [PDF]