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Brain Res. 1998 Jul 6;798(1-2):7-17.

Systemically administered cocaine alters stimulus-evoked responses of thalamic somatosensory neurons to perithreshold vibrissae stimulation.

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  • 1Department of Neurobiology and Anatomy, Allegheny University of the Health Sciences, Philadelphia, PA 19102-1192, USA.


Previous studies have shown that systemically administered cocaine can transiently alter responses of primary somatosensory cortical neurons to threshold level stimulation of peripheral receptive fields. The goal of the present investigation was 2-fold: (1) characterize the effects of systemic cocaine on stimulus-evoked responses of the ventral posterior medial (VPM) thalamic neurons which relay somatosensory information to the cortex and (2) determine the time course and magnitude of changes in monoamine levels within the somatosensory thalamus following systemic administration of cocaine. Extracellularly recorded responses of single VPM thalamic neurons to whisker stimulation were monitored before and after cocaine administration in halothane anaesthetized rats. Each cell was first characterized by assessing its response profile to a range of perithreshold level deflections of the optimal whisker on the contralateral face. Drug effects on stimulus-response curves, response magnitude and latency were determined from quantitative analysis of spike train data. The results indicate that cocaine elicits a predictable augmentation or attenuation of the sensory response magnitude, with the direction of the change inversely related to the initial magnitude of the stimulus-evoked discharge. In addition, cocaine consistently reduced the response time of somatosensory thalamic neurons to peripheral receptive field stimulation. At the same dose and over the same time period, cocaine also produced marked elevation of norepinephrine and serotonin levels within the ventrobasal thalamus, as determined by in vivo microdialysis. These results suggest that cocaine-induced increases in norepinephrine and serotonin are responsible for drug-related modulation of the transfer of sensory signals through primary thalamocortical relay circuits.

Copyright 1998 Elsevier Science B.V. All rights reserved.

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