Anorexigenic C75 alters c-Fos in mouse hypothalamic and hindbrain subnuclei

Ian Miller, Gabriele V. Ronnett, Timothy H. Moran, Susan Aja

Research output: Contribution to journalArticlepeer-review


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 languageEnglish (US)
Pages (from-to)925-929
Number of pages5
Issue number5
StatePublished - Apr 9 2004


  • 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

  • Neuroscience(all)


Dive into the research topics of 'Anorexigenic C75 alters c-Fos in mouse hypothalamic and hindbrain subnuclei'. Together they form a unique fingerprint.

Cite this