Ventromedial hypothalamic mediation of sucrose feeding induced pain modulation

Citation
K. Mukherjee et al., Ventromedial hypothalamic mediation of sucrose feeding induced pain modulation, PHARM BIO B, 68(1), 2001, pp. 43-48
Citations number
38
Categorie Soggetti
Neurosciences & Behavoir
Journal title
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
ISSN journal
00913057 → ACNP
Volume
68
Issue
1
Year of publication
2001
Pages
43 - 48
Database
ISI
SICI code
0091-3057(200101)68:1<43:VHMOSF>2.0.ZU;2-Y
Abstract
Electrophysiological and behavioural studies suggest a modulatory role of v entromedial nucleus of the hypothalamus (VMH) in nociceptive behaviour. Les ion of the VMH produces hyperalgesia and a greater preference for sucrose s olution. Hyperalgesia is also produced by sucrose feeding. To explore speci fically the contribution of glucoreceptor neurons of the VMH in the mediati on of sucrose-fed hyperalgesia, 2-deoxy-D-glucose (2-DG, antimetabolite of glucose) was slowly albeit continuously infused (1 mul/h for 7 days by micr oinfusion pumps) into the VMH of adult male rats. Simultaneously, the rats underwent tests for their nociceptive responses in control and sucrose-fed states. The tests for nociception, namely, tail flick latency (TFL), thresh olds of tail flick (TF), vocalization during stimulus (SV), vocalization af ter discharge (VA) were recorded at 0500 h. The tests were repeated after 6 , 12, and 38 h in 1 M saline (control group) and 2-DG (experimental group) microinfused rats. Rats were presented with sucrose (20%) solution for 48 h at 0500 h ad libitum in addition to food pellets and tap water. Infusion o f 2-DG per se in the VMH led to hypoalgesia tin threshold of TF, SV. VA) wh ile feeding sucrose for 6-12 h per se led to hyperalgesia tin TFL, threshol d of SV and VA). Sucrose feeding to 2-DG rats, however, attenuated the hypo algesia of 2-DG as well as the hyperalgesia of sucrose feeding. The results suggest that the VMH glucoreceptor neurons probably modulate sucrose media ted phasic pain responses. (C) 2000 Elsevier Science Inc. All rights reserv ed.