Site-specific attenuation of food intake but not the latency to eat after hypothalamic injections of neuropeptide Y in dehydrated-anorexic rats

Abstract

Anorexia that accompanies cellular dehydration in rats (DE-anorexia) offers a relatively simple model for investigating the functional organization of neural mechanisms that can suppress feeding during dehydration. Previous studies strongly suggest that the inputs that drive ingestive behavior control neurons in the paraventricular nucleus of the hypothalamus (PVH) and lateral hypothalamic area (LHA) remain active during DE-anorexia. Here we examine whether these two regions retain their sensitivity to neuropeptide Y (NPY). NPY is an important component in two major feeding-related inputs from the arcuate nucleus and the hindbrain. We found that intake responses to NPY injections in the LHA and PVH were suppressed in DE-anorexia, but the PVH remained less sensitive to the effects of NPY than the LHA in DE-anorexic animals. Indeed the higher dose of NPY (238 pmol) completely overcame shorter periods of DE-anorexia when injected into the LHA but not the PVH. However, the latency to eat after NPY injections remained unchanged from control animals, regardless of NPY dose, injection location, or intensity of anorexia. Furthermore, the onset and size of the strong and rapidly induced compensatory feeding that follows the return of water to DE-anorexic animals was also unaffected by any NPY injections. These data support the hypothesis that DE-anorexia develops as a consequence of the premature termination of regularly initiated meals, which perhaps involves processes that alter the sensitivity of satiety mechanisms downstream to the PVH and LHA.

Dehydration-anorexia derives from a reduction in meal size, but not meal number

“…Our results demonstrate that DE-anorexia derives from a reduction in meal size while the number of daily meals is virtually unchanged. This pattern is consistent with the hypothesis we have previously proposed where meal initiation is unimpeded, but meals are terminated prematurely [1, 15]. We also find that as drinking HS continues fewer meals are taken during the dark period and more are taken during the light period, an adaptation that persists for some days following the return of drinking water.…”

Chronic dehydration affects hydroelectrolytic equilibrium and adrenal gland morphology in wistar rat: comparison with <i>Gerbillus tarabuli</i>

“…The weight lost recorded in dehydrated rats can be attributed to the reduced body fluids, as it was estimated by Van Bauman's formula (result not shown), and partially to a reduction in food consumption (personnel observations), which leads ultimately to tissue catabolism. Indeed, our observation is supported by experimental evidence showing that rats submitted to similar conditions developed anorexia [14][15].…”

The functional architecture of dehydration-anorexia

“…Further evidence for this model comes from the response of DE-anorexic animals to local injections of NPY into the PVH or LHA [20]. NPY is a neuropeptide found in some ARH and hindbrain catecholaminergic neurons that project to the LHA and PVH [20,23].…”

“…NPY is a neuropeptide found in some ARH and hindbrain catecholaminergic neurons that project to the LHA and PVH [20,23]. NPY acts to increase feeding by directing an animal's foraging behavior towards food and by reducing the efficacy of satiety signals that terminate feeding [21,22].…”

“…DE-anorexic animals injected with NPY into the PVH or LHA initiate feeding with the same latency as controls (7 – 9 minutes), but the amount of food consumed over the next hour is significantly reduced [20]. The reduced efficacy of NPY to stimulate feeding in DE-anorexic animals is site-specific; the LHA remains more sensitive to NPY than the PVH.…”