Abstract
Focal electrical stimulation of the arcuate nucleus of the hypothalamus (ARH) for 5 min (1 session) produced a marked elevation of tail flick latency (TFL) to noxious heat in the pentobarbital-anesthetized rat. Repeated stimulation for a total of 11 sessions at 30 min intervals resulted in a gradual decline in the hypoalgesic action, and this tolerance may last for 7 days. Tolerance to the ARH analgesic stimulation reduced the analgesia produced by low (2 Hz) but not high (100 Hz) frequency electroacupuncture (EA); and tolerance to low frequency EA analgesia attenuated the ARH stimulation-produced analgesia without affecting high frequency EA analgesia. Alternatively, rats tolerant to high-frequency EA analgesia were still sensitive to either the ARH or low-frequency EA stimulation. These results suggest that the ARH stimulation and low-frequency EA administration produced analgesia via a common neural mechanism, supporting our hypothesis put forward previously that the ARH plays an important role in mediating low- but not high-frequency EA analgesia.
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