Effect of VMH lesion on sucrose-fed nociceptive responses

An initial analgesia followed by hyperalgesia to phasic noxious stimuli occ urs after ingestion of sucrose ad libitum. However, the mechanism underlyin g hyperalgesia is not known. The present study was designed to explore the role of VMH in the mediation of the hyperalgesic effect of sucrose ingestio n. Adult male albino rats received sucrose solution (20% p.o,) in addition to laboratory food pellets and tap water ad libitum. Their behavioural resp onses to various phasic and tonic noxious stimuli were recorded after 6, 12 and 48 h during pre and post-sucrose fed states in both the control and VM H lesion groups of rats. Sucrose feeding to control rats significantly redu ced the tail flick latency (TFL) and threshold of vocalization during stimu lus (SV) and after discharge (VA) indicating hyperalgesia, while the thresh old of tail flick remained unaffected. The average pain rating during the f ormalin test (tonic pain) decreased significantly indicating analgesia. VMH lesion decreased the latency (mean+/-SD) for tail flick (11.26+/-4.65 from 15.61+/-5.12 s), threshold (median) for tail flick (0.04 from 0.08 mA), vo calization during stimulus (0.05 from 0.1 mA) and vocalization after discha rge (0.15 from 0.2 mA), while the tonic pain rating increased, thereby sugg esting a hyperalgesic state. However, sucrose feeding to lesioned rats neit her potentiated nor attenuated their hyperalgesia. The results suggest that sucrose feeding for 6-48 h ad libitum produces hyperalgesia to phasic noxi ous and analgesia to tonic noxious stimuli, while VMH lesion produces hyper algesia to both phasic and tonic noxious stimuli. Secondly, sucrose ingesti on by VMH lesion rats does not affect their responses to pain, suggesting t he possible role of VMH in the mediation of sucrose-fed nociceptive respons es.