The hypothesis that acutely administered ethanol could interfere with neocortical recurrent inhibition (RI) was supported. The large surface negative wave in response to antidromic stimulation of the cerebral peduncle represents a summation of inhibitory postsynaptic potentials, a measure of RI. In acute experiments on adult rats, blood alcohol levels of less than about 120 mg/100 ml slightly facilitated the surface negative wave. Higher blood alcohol levels always blocked the surface negative response. Stimulation of the somatosensory thalamic relay nuclei produced a cortical response on which ethanol had a moderate blocking effect. Conditioning-test procedures revealed that cerebral peduncle stimulation strongly blocked the thalamocortical (test) response, especially after ethanol, but thalamic stimulation (conditioning) had no effect upon the surface negative wave. This demonstrates a differential effect on the two cortical processes. Cortical RI seems to be especially sensitive to blood alcohol level, but the function of cortical RI is complex. By way of acting on RI, ethanol likely affects control of sensory input and cortical sensory organization as well as selectivity and magnitude of motor discharge.