Cocaine-induced vs. behaviour-related alterations of spontaneous and evoked discharge of somatosensory cortical neurons.

While the abuse potential of cocaine stems mainly from its ability to increase dopaminergic transmission in limbic regions, drug actions on other monoamine-innervated circuits may contribute to the development and maintenance of cocaine addiction. Previous extracellular recordings in anaesthetized rats revealed a facilitatory influence of cocaine on primary sensory pathways, which could influence the processing of drug-related stimuli during the development of cocaine addiction. We further analysed these sensory effects of cocaine in freely behaving rats (n = 9). Using an array of eight microelectrodes chronically implanted in infragranular layers of primary somatosensory cortex, we recorded the basal activity of 40 single- and 64 multiunits and their response to electrical stimulation of the whisker pad before and after incremental doses of cocaine (0.25-2 mg/kg i.v.). Both spontaneous and cocaine-induced explorations were associated with elevated basal firing of the cortical neurons and suppression of their short-latency excitation and postexcitatory inhibition in response to the whisker-pad stimulation. In addition to exploration-related alterations, the administration of cocaine enhanced the long-latency rebound excitation induced by the whisker-pad stimulation. This component of the sensory response, which is more labile and does not seem to convey information about the physical characteristics of the stimulus, may participate in the processing of drug-related sensory stimuli.