Propensity to form conditioned taste aversions augments anorexia in obese (ob/ob) mice with B16 melanoma.

Ob/ob mice (OB) with B16 melanoma become anorectic, but lean mice (LN) do not. Present studies suggest that this difference reflects a greater bent for OB to form conditioned taste aversions (CTA). In Exp 1, healthy OB formed stronger CTAs than LN to a saccharin taste paired with lithium chloride (LiCl, 3 mEq/kg ip).

Dysregulation of the Hypothalamus-Pituitary-Adrenal Axis in Male and Female, Genetically Obese (ob/ob) Mice.

The autosomal, recessive obesity of ob/ob mice is associated with hypercorticosteronemia and amelioration of most symptoms of obesity following adrenalectomy. Increased adrenocorticotropic hormone (ACTH) secretion has been hypothesized on the basis of several reports of higher pituitary ACTH content in ob/ob mice compared to lean littermates. However, the only measurement of ACTH blood concentration found lower levels in ob/ob mice than in leans suggesting that hypercorticosteronemia might result solely from an enhanced adrenal response to ACTH and also suggesting that the ob/ob's elevated pituitary ACTH content might be due to decreased ACTH secretion rather than increased ACTH synthesis.

Reduction of learned helplessness by central administration of quaternary naltrexone.

Prior research has established that escape impairment resulting from prior inescapable shock (IS) could be reversed by the peripheral administration of the opiate antagonist naltrexone (NTX), but not the quaternary form of naltrexone (QNTX), which when systemically administered, does not readily pass the blood-brain barrier. As it was unclear whether the failure of systemically administered QNTX to reduce shuttle escape deficits following exposure to IS could be attributed to reasons other than the restricted access of QNTX to receptor sites in the brain, rats were affixed with chronic indwelling ventricular cannulae to allow direct brain administration of QNTX. The present experiment found a significant attenuation of the escape deficit produced by prior inescapable shock following the intracerebroventricular (ICV) administration of QNTX (10 micrograms/rat).

Central mediation of naloxone-induced anorexia in the ventral tegmental area.

Central naloxone injections were used to show that endogenous opioids in the ventral tegmental area (VTA) regulate consumption of palatable foods. Peripheral injections of naloxone were more effective in reducing the consumption of a sweet solution in normally fed rats than in animals maintained at 85% of their free-feeding body weight. A dose of 10 micrograms/side naloxone injected into the VTA reduced consumption in normally fed rats, whereas a dose of 25 micrograms/side did the same in food-restricted animals.

Genetically obese (ob/ob) mice are hypersensitive to glucocorticoid stimulation of feeding but dramatically resist glucocorticoid-induced weight loss.

The genetically obese (ob/ob) mouse is hyperphagic and hypercorticosteronemic; both hyperphagia and excessive weight gain are ameliorated by adrenalectomy. We report here that corticosterone or dexamethasone stimulate feeding in obese mice at one-fifth the dose needed to increase feeding in lean littermates. Metabolic weight loss, a measure of carbon dioxide and water lost due to respiration, is stimulated by glucocorticoids.