Electrolytic lesions of central gray matter (CGM) were induced in rats. The analgesia produced by stress (foot shock) tested by the hot-plate and tail-flick method was significantly and substantially reduced in the lesioned rats. The baseline pain threshold measured by the hot-plate method was significantly longer in CGM-lesioned rats. The baseline tail-flick latency was unaffected by the lesions. The role of CGM in the regulation of pain sensitivity in rats is discussed.