The role of hypothalamic ingestive behavior controllers in generating dehydration anorexia: a Fos mapping study.
Giving rats 2.5% saline to drink for 3-5 days simply and reliably generates anorexia. Despite having the neurochemical and hormonal markers of negative energy balance, dehydrated anorexic rats show a marked suppression of spontaneous food intake, as well as the feeding that is usually stimulated by overnight starvation or a 2-deoxy-d-glucose (2DG) challenge. These observations are consistent with a dehydration-dependent inhibition of the core circuitry that controls feeding. We hypothesize that this inhibition is directed at those neurons in the paraventricular nucleus and lateral hypothalamic area that constitute the hypothalamic "behavior controller" for feeding rather than their afferent inputs from the arcuate nucleus or hindbrain that convey critical feeding-related sensory information. To test this hypothesis, we mapped and quantified the Fos-immunoreactive response to 2DG in control and dehydrated rats drinking 2.5% saline. Our rationale was that regions showing an attenuated Fos response to 2DG in dehydrated animals would be strong candidates as the targets of dehydration-induced suppression of 2DG feeding. We found that the Fos response to combined dehydration and 2DG was attenuated only in the lateral hypothalamic area, with dehydration alone increasing Fos in the lateral part of the paraventricular nucleus. In the arcuate nucleus and those regions of the hindbrain that provide afferent inputs critical for the feeding response to 2DG, the Fos response to 2DG was unaffected by dehydration. Therefore, dehydration appears to target the lateral hypothalamic area and possibly the lateral part of the paraventricular nucleus to suppress the feeding response to 2DG.
Salter-Venzon
Dawna
D
The Neuroscience Graduate Program and The Department of Biological Sciences, University of Southern California (USC) College, USC, Los Angeles, California 90089-2520, USA.
Watts
Alan G
AG
D000818:Animals; D000855:Anorexia / Q000209:etiology* / Q000378:metabolism; D001111:Arcuate Nucleus of Hypothalamus / Q000187:drug effects / Q000502:physiology; D031608:Area Postrema / Q000187:drug effects / Q000502:physiology; D003681:Dehydration / Q000139:chemically induced / Q000150:complications* / Q000378:metabolism; D003847:Deoxyglucose / Q000494:pharmacology; D005247:Feeding Behavior / Q000187:drug effects / Q000502:physiology*; D007026:Hypothalamic Area, Lateral / Q000187:drug effects / Q000502:physiology; D007031:Hypothalamus / Q000187:drug effects / Q000502:physiology*; D008297:Male; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000502:physiology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012462:Saline Solution, Hypertonic / Q000494:pharmacology; D017552:Solitary Nucleus / Q000187:drug effects / Q000502:physiology
D016760:Proto-Oncogene Proteins c-fos; D012462:Saline Solution, Hypertonic; D003847:Deoxyglucose