Abstract
The fatty acid synthase inhibitor C75 reduces feeding rapidly and for several days. We investigated brain sites potentially involved in actions of i.p. C75 in mice by examining c-Fos. At 3 h C75 increased numbers of c-Fos-immunoreactive cells in hindbrain feeding-related nuclei, and in the paraventricular nucleus (PVN), lateral aspects of the arcuate nucleus (ARC), and in the central amygdala. At 24 h C75 prevented fasting-induced c-Fos expression in the medial ARC and three of its targets: lateral magnocellular PVN, lateral hypothalamus, and dorsomedial hypothalamus. C75, but not fasting, increased c-Fos in parvocellular PVN. This pattern of results suggests a shift from hindbrain-initiated short-term actions to activation of hypothalamic mechanisms that could mediate the long-term anorectic responses to C75.
Original language | English (US) |
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Pages (from-to) | 925-929 |
Number of pages | 5 |
Journal | Neuroreport |
Volume | 15 |
Issue number | 5 |
DOIs | |
State | Published - Apr 9 2004 |
Keywords
- Arcuate nucleus
- Area postrema
- Central nucleus of amygdala
- Dorsomedial hypothalamus
- Food intake
- Lateral hypothalamus
- Nucleus of solitary tract
- Parabrachial nucleus
- Paraventricular nucleus
ASJC Scopus subject areas
- General Neuroscience