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 go
al of the present investigation was 2-fold: (1) characterize the effec
ts of systemic cocaine on stimulus-evoked responses of the ventral pos
terior medial (VPM) thalamic neurons which relay somatosensory informa
tion to the cortex and (2) determine the time course and magnitude of
changes in monoamine levels within the somatosensory thalamus followin
g systemic administration of cocaine. Extracellularly recorded respons
es of single VPM thalamic neurons to whisker stimulation were monitore
d before and after cocaine administration in halothane anaesthetized r
ats. Each cell was first characterized by assessing its response profi
le to a range of perithreshold level deflections of the optimal whiske
r on the contralateral face. Drug effects on stimulus-response curves,
response magnitude and latency were determined from quantitative anal
ysis of spike train data. The results indicate that cocaine elicits a
predictable augmentation or attenuation of the sensory response magnit
ude, with the direction of the change inversely related to the initial
magnitude of the stimulus-evoked discharge. In addition, cocaine cons
istently reduced the response time of somatosensory thalamic neurons t
o peripheral receptive field stimulation. At the same dose and over th
e same time period, cocaine also produced marked elevation of norepine
phrine and serotonin levels within the ventrobasal thalamus, as determ
ined by in vivo microdialysis. These results suggest that cocaine-indu
ced increases in norepinephrine and serotonin are responsible for drug
-related modulation of the transfer of sensory signals through primary
thalamocortical relay circuits. (C) 1998 Elsevier Science B.V. All ri
ghts reserved.