Abstract
Obesity may result from dysfunction of the reward system, especially in the nucleus accumbens (Acb). Based on this hypothesis, many researchers have tested the effect of high-frequency stimulation (HFS) of the Acb shell (Acb-Sh) and/or core (Acb-Co) on ingestive behaviors, but few studies have explored the possible mechanisms involved in the differences between the Acb-Sh and Acb-Co. The present study tested effects of HFS of the Acb-Sh and Acb-Co on high-fat food (HFF) consumption in rats after 24h of food deprivation. Microdialysis and electrophysiological experiments were carried out in awake rats to explore potential mechanisms. The results showed that the Acb-Sh decreased HFF consumption after food deprivation both during and post-HFS. However, HFS of the Acb-Co did not induce similar changes in food consumption. HFS of the Acb-Sh (Sh-HFS) induced an increase in GABA level in the lateral hypothalamic area (LHA) during both phases, whereas HFS of the Acb-Co (Co-HFS) did not exhibit similar effects. The electrophysiological experiment showed that nearly all the LHA neurons were inhibited by Sh-HFS, and the mean firing rate decreased significantly both during and post-HFS. In contrast, the mean firing rate of the LHA neurons did not exhibit clear changes during Co-HFS, although some individual neurons appeared to exhibit responses to Co-HFS. Considering all the data, we postulated that Sh-HFS, rather than Co-HFS, might inhibit palatable food consumption after food deprivation by decreasing the reward value of that food, which suggested that it might also disturb the process of developing obesity. The mechanisms involved in the different effects of Sh-HFS and Co-HFS on food consumption may be associated with different neural responses in the LHA. The Acb-Sh has abundant GABAergic projections to the LHA, whereas the Acb-Co has few or no GABAergic innervations to the LHA. Thus, neural activity in the LHA exhibits different responses to Sh-HFS and Co-HFS.
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