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 hallucinations. Although many studies have examined the cellular actions of cocaine in "reward" circuits of the brain, few have investigated the impact of cocaine on neuronal function in primary sensory circuits. The goal of this study was to characterize the effects of cocaine on somatosensory cortical neuronal responsiveness to peripheral activation of afferent synaptic pathways. Extracellular recordings were obtained from spontaneously active single units in the barrel field cortex of halothane-anesthetized rats. The spontaneous firing rate and cellular responses to mechanical displacement of a single whisker on the contralateral 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 whisker stimulation consisted of an initial excitatory burst (E1), a postexcitatory suppression of activity (I) and a secondary excitatory discharge (E2). Cocaine effects on spontaneous discharge were minimal at low doses up to and including 1.0 mg/kg, whereas suppression of spontaneous activity was observed at doses above 2.0 mg/kg. After cocaine injection, E1 responses were unchanged or within +/- 30% of control; however, E2 responses were routinely enhanced 50% to 600% above control levels. I responses were increased in magnitude and/or duration. Such facilitation of E2 and I responses was observed at doses as low as 0.25 mg/kg but most consistently at doses of 0.5 to 1.0 mg/kg. Suppression of evoked responses was observed at doses above 2.0 mg/kg. Cocaine's effects on spontaneous and evoked discharge were rapid in onset. Peak effects occurred at 6 min postinjection and recovery to control patterns of discharge were observed by 20 min postinjection. These results indicate that cocaine consistently exerts a facilitating effect on specific late components of cortical neuron responses to sensory stimuli. Although the neural substrates responsible for this effect have not been identified, such findings demonstrate a clear effect of cocaine on sensory signal transmission at dosages that can support behavioral reinforcement.
Bekavac
I
I
Department of Physiology and Biophysics, Hahnemann University, Philadelphia, Pennsylvania.
Waterhouse
B D
BD
D000818:Animals; D003042:Cocaine / Q000494:pharmacology*; D005071:Evoked Potentials / Q000187:drug effects; D008297:Male; D011343:Procaine / Q000494:pharmacology; D051381:Rats; D013003:Somatosensory Cortex / Q000187:drug effects*; D013997:Time Factors; D014738:Vibrissae / Q000502:physiology*
D011343:Procaine; D003042:Cocaine