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This Article Full Text Full Text (PDF) All Versions of this Article: 584/2/565    most recent jphysiol.2007.141135v1 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 Google Scholar Google Scholar Articles by Kasten, M. R. Articles by Anderson, M. P. Search for Related Content PubMed PubMed Citation Articles by Kasten, M. R. Articles by Anderson, M. P. Related Collections Neuroscience

¹ Departments of Neurology and Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
² Departments of Physiology, Neuroscience, and Biochemistry, New York University School of Medicine, New York, NY 10016, USA

Sensory signals of widely differing dynamic range and intensity are transformed into a common firing rate code by thalamocortical neurons. While a great deal is known about the ionic currents, far less is known about the specific channel subtypes regulating thalamic firing rates. We hypothesized that different K⁺ and Ca²⁺ channel subtypes control different stimulus–response curve properties. To define the channels, we measured firing rate while pharmacologically or genetically modulating specific channel subtypes. Inhibiting Kv3.2 K⁺ channels strongly suppressed maximum firing rate by impairing membrane potential repolarization, while playing no role in the firing response to threshold stimuli. By contrast, inhibiting Kv1 channels with -dendrotoxin or maurotoxin strongly increased firing rates to threshold stimuli by reducing the membrane potential where action potentials fire (V_th). Inhibiting SK Ca²⁺-activated K⁺ channels with apamin robustly increased gain (slope of the stimulus–response curve) and maximum firing rate, with minimum effects on threshold responses. Inhibiting N-type Ca²⁺ channels with -conotoxin GVIA or -conotoxin MVIIC partially mimicked apamin, while inhibiting L-type and P/Q-type Ca²⁺ channels had small or no effects. EPSC-like current injections closely mimicked the results from tonic currents. Our results show that Kv3.2, Kv1, SK potassium and N-type calcium channels strongly regulate thalamic relay neuron sensory transmission and that each channel subtype controls a different stimulus–response curve property. Differential regulation of threshold, gain and maximum firing rate may help vary the stimulus–response properties across and within thalamic nuclei, normalize responses to diverse sensory inputs, and underlie sensory perception disorders.

(Received 20 July 2007; accepted after revision 28 August 2007; first published online 30 August 2007)
Corresponding author M. P. Anderson: Department of Neurology, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. Email: mpanders{at}bidmc.harvard.edu

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