SYSTEMICALLY ADMINISTERED COCAINE SELECTIVELY ENHANCES LONG-LATENCY RESPONSES OF RAT BARREL FIELD CORTICAL-NEURONS TO VIBRISSAE STIMULATION

Prominent among cocaine's psychostimulant actions are its abilities to heighten awareness of the sensory surround and induce sensory halluci nations. Although many studies have examined the cellular actions of c ocaine in ''reward'' circuits of the brain, few have investigated the impact of cocaine on neuronal function in primary sensory circuits. Th e goal of this study was to characterize the effects of cocaine on som atosensory cortical neuronal responsiveness to peripheral activation o f afferent synaptic pathways. Extracellular recordings were obtained f rom spontaneously active single units in the barrel field cortex of ha lothane-anesthetized rats. The spontaneous firing rate and cellular re sponses to mechanical displacement of a single whisker on the contrala teral face were monitored before and after systemic administration of cocaine (0.25, 0.5, 1.0 and 2.0 mg/kg i.v.). Control responses to whis ker stimulation consisted of an initial excitatory burst (El), a poste xcitatory suppression of activity (I) and a secondary excitatory disch arge (E2). Cocaine effects on spontaneous discharge were minimal at lo w doses up to and including 1.0 mg/kg, whereas suppression of spontane ous activity was observed at doses above 2.0 mg/kg. After cocaine inje ction, El responses were unchanged or within +/- 30% of control; howev er, E2 responses were routinely enhanced 50% to 600% above control lev els. I responses were increased in magnitude and/or duration. Such fac ilitation of E2 and I responses was observed at doses as low as 0.25 m g/kg but most consistently at doses of 0.5 to 1.0 mg/kg. Suppression o f evoked responses was observed at doses above 2.0 mg/kg. Cocaine's ef fects on spontaneous and evoked discharge were rapid in onset. Peak ef fects occurred at 6 min postinjection and recovery to control patterns of discharge were observed by 20 min postinjection. These results ind icate that cocaine consistently exerts a facilitating effect on specif ic late components of cortical neuron responses to sensory stimuli. Al though the neural substrates responsible for this effect have not been identified, such findings demonstrate a clear effect of cocaine on se nsory signal transmission at dosages that can support behavioral reinf orcement.