Characterization of inhibition of spinal nociceptive reflex by stimulation of the arcuate nucleus of the hypothalamus in the pentobarbital-anesthetized rat.

The effects of electrical and chemical stimulation of the arcuate nucleus of the hypothalamus (ARH) on the tail flick latency (TFL) and paw pressure withdrawal threshold (PWT) were investigated in the lightly pentobarbital-anesthetized and acutely prepared rat. Electrical stimulation of the ARH for 20 sec at 8 Hz produced a more potent elevation of the TFL (98%) and PWT (68%) compared to when stimulation was applied to the same site at 2 Hz (41% and 25%, respectively), 32 Hz (64% and 42%) and 128 Hz (57% and 39%). An even more marked and longer attenuation of the nociceptive reflexes was observed when the ARH stimulation was extended to a period of 1 or 3 min. Microinjection of the excitant amino acid, L-glutamate (0.5 M, 0.1 mul), into the same areas of the ARH consistently elicited antinociception to an extent similar to that observed with electrical stimulation. The data indicate that 8 Hz seems to be an optimal frequency for stimulating ARH to produce an analgesic effect as tested by the two spinal nociceptive reflexes.