The present study investigates the effects of the 5-hydroxytryptamine1A agonist ipsapirone on electroencephalography and somatosensory evoked potentials after middle cerebral artery occlusion in the rat. We implanted 17 silver ball electrodes symmetrically distributed over the skull in 14 rats and registered electroencephalography activity and somatosensory evoked potentials before, 1 hour, and 1 week after permanent occlusion of the left middle cerebral artery. Before vessel occlusion, a symmetric distribution of electroencephalography power was seen over both hemispheres. Middle cerebral artery occlusion caused a complete abolishment of electroencephalography power in the frontolateral aspects of the affected hemisphere. When electroencephalographic recordings 7 days after the insult were superimposed with three-dimensional-reconstructed pictures of the infarct, a close correspondence of the extention and spatial orientation was noted. Two negative and two positive peaks were consistently recorded before middle cerebral artery occlusion. In both control and ipsapirone-treated (30 mg/kg i.p. 30 minutes after induction of ischemia) animals, the vessel occlusion caused a severe reduction in amplitudes of somatosensory evoked potentials in all areas under record (p less than 0.05). One week after middle cerebral artery occlusion, amplitudes of somatosensory potentials over the lesioned hemisphere were still significantly (p less than 0.05) lower than preischemic values in the control group. When compared with the corresponding values 1 hour after middle cerebral artery occlusion, an albeit insignificant tendency toward increased amplitudes was observed in most areas under record. By contrast, in ipsapirone-treated animals, significant differences compared with preischemic values were no longer present 1 week after the vessel occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)