Forebrain patterns of c-Fos and FosB induction during cancer-associated anorexia-cachexia in rat.
European Journal of Neuroscience. 2005-05-01; 21(10): 2752-2766
DOI: 10.1111/j.1460-9568.2005.04102.x
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1. Eur J Neurosci. 2005 May;21(10):2752-66.
Forebrain patterns of c-Fos and FosB induction during cancer-associated
anorexia-cachexia in rat.
Konsman JP(1), Blomqvist A.
Author information:
(1)Department of Cell Biology, Faculty of Health Sciences, University of
Linköping, S-581 85 Linköping, Sweden.
Forebrain structures are necessary for the initiation of food intake and its
coupling to energy expenditure. The cancer-related anorexia-cachexia syndrome is
typified by a prolonged increase in metabolic rate resulting in body weight loss
which, paradoxically, is accompanied by reduced food intake. The aim of the
present work was to study the forebrain expression of Fos proteins as activation
markers and thus to identify potential neurobiological mechanisms favouring
catabolic processes or modulating food intake in rats suffering from
cancer-related anorexia-cachexia. Neurons in forebrain structures showing most
pronounced induction of Fos proteins were further identified neurochemically. To
provoke anorexia-cachexia, cultured Morris hepatoma 7777 cells were injected
subcutaneously in Buffalo rats. This resulted in a slowly growing tumour inducing
approximately 7% body weight loss and a 20% reduction in food intake when the
tumour represented 1-2% of body mass. Anorexia-cachexia in these animals was
found to be accompanied by Fos induction in several hypothalamic nuclei including
the paraventricular and ventromedial hypothalamus, in the parastrial nucleus, the
amygdala, the bed nucleus of the stria terminalis, ventral striatal structures
and the piriform and somatosensory cortices. Neurochemical identification
revealed that the vast majority of FosB-positive neurons in the nucleus
accumbens, ventral caudate-putamen and other ventral striatal structures
contained prodynorphin or proenkephalin mRNA. These findings indicate that
forebrain structures that are part of neuronal networks modulating catabolic
pathways and food ingestion are activated during tumour-associated
anorexia-cachexia and may contribute to the lack of compensatory eating in
response to weight loss characterizing this syndrome.
DOI: 10.1111/j.1460-9568.2005.04102.x
PMID: 15926923 [Indexed for MEDLINE]