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This Article Full Text Full Text (PDF) All Versions of this Article: 95/3/1735    most recent 00734.2005v1 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 Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Golomb, D. Articles by Kleinfeld, D. Search for Related Content PubMed PubMed Citation Articles by Golomb, D. Articles by Kleinfeld, D.

Coding of Stimulus Frequency by Latency in Thalamic Networks Through the Interplay of GABA_B-Mediated Feedback and Stimulus Shape

¹Center for Theoretical Biological Physics; ²Department of Physics; ³Graduate Program in Neurosciences, University of California San Diego, La Jolla, California; ⁴Department of Physiology and Zlotowski Center for Neuroscience, Ben Gurion University of the Negev, Beer-Sheva; and ⁵Department of Neurobiology, The Weizmann Institute of Science, Rehovot, Israel

Submitted 12 July 2005; accepted in final form 26 October 2005

A temporal sensory code occurs in posterior medial (POm) thalamus of the rat vibrissa system, where the latency for the spike rate to peak is observed to increase with increasing frequency of stimulation between 2 and 11 Hz. In contrast, the latency of the spike rate in the ventroposterior medial (VPm) thalamus is constant in this frequency range. We consider the hypothesis that two factors are essential for latency coding in the POm. The first is GABA_B-mediated feedback inhibition from the reticular thalamic (Rt) nucleus, which provides delayed and prolonged input to thalamic structures. The second is sensory input that leads to an accelerating spike rate in brain stem nuclei. Essential aspects of the experimental observations are replicated by the analytical solution of a rate-based model with a minimal architecture that includes only the POm and Rt nuclei, i.e., an increase in stimulus frequency will increase the level of inhibitory output from Rt thalamus and lead to a longer latency in the activation of POm thalamus. This architecture, however, admits period-doubling at high levels of GABA_B-mediated conductance. A full architecture that incorporates the VPm nucleus suppresses period-doubling. A clear match between the experimentally measured spike rates and the numerically calculated rates for the full model occurs when VPm thalamus receives stronger brain stem input and weaker GABA_B-mediated inhibition than POm thalamus. Our analysis leads to the prediction that the latency code will disappear if GABA_B-mediated transmission is blocked in POm thalamus or if the onset of sensory input is too abrupt. We suggest that GABA_B-mediated inhibition is a substrate of temporal coding in normal brain function.

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