Abstract
Areas (3) within the periventricular system were studied: caudal periaqueductal gray (PAG), rostral PAG, and caudal midline thalamus. Rats were chronically prepared with a bipolar stimulating electrode in 1 of these areas and 2 lesion electrodes in another. Current thresholds for stimulation-produced analgesia in the tail-flick test were assessed. Lesions were made and thresholds for analgesia re-assessed. Destruction of the caudal PAG consistently produced large increases in thresholds for analgesia at rostral stimulation sites; destruction of the rostral areas did not affect thresholds at caudal PAG sites. Lesions in all 3 areas yielded significant reductions in baseline (pre-brain stimulation) tail-flick latencies. Both sham lesioned control animals and animals with small lesions maintained stable baseline latencies and analgesia thresholds. All 3 brain areas studied contribute to the same pain-inhibitory system. Stimulation at rostral sites activates elements which connect to or pass through the caudal PAG.