Effect of VMH lesion on sucrose-fed analgesia in formalin pain.

Abstract

The ingestion of sucrose (ad libitum) produces an immediate analgesic response to phasic noxious stimuli. The underlying mechanism for the analgesic effect of sucrose is attributed to its palatability, which mediates analgesia probably by the release of beta-endorphin in the hypothalamus. The present study was designed to explore the role of ventromedial hypothalamus in the mediation of sucrose-fed analgesia. Adult male albino rats each received (20%) sucrose solution orally through a separate bottle until they had ingested 4-5 ml. Their behavioral responses to tonic noxious stimulus in a formalin test were studied in pre- and postsucrose-fed rats of control and in the VMH lesion groups. The average pain rating of a 60-min session significantly (p < 0.01) decreased after sucrose feeding in control rats, from 1.94 +/- 0.13 to 1.45 +/- 0.14, but sucrose feeding by the VMH lesion rats did not alter their tonic nociceptive response from a 1.70 +/- 0.07 presucrose-fed state to a 1.71 +/- 0.08 postsucrose-fed state. VMH lesion per se did not alter the nociceptive response in comparison with controls. The results suggest that sucrose feeding produces analgesia to tonic noxious stimulus, which is abolished by lesion of the VMH, thereby indicating a significant role of VMH in sucrose-fed analgesia.