Hypothalamic hyperphagia prevented by damage to brain dopamine-containing neurons.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S M Antelman.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The proposed hypothesis is directed toward explaining a number of disparate findings in terms of a stress-related interaction between the NE- and DA-containing systems in the brain. The deleterious behavioral effects of decreased DA activity, for example, may be counterbalanced by a similar decrease occurring in NE activity, such compensation being most likely to occur under conditions of stress. This hypothesis may have application to the understanding of neurological and mental disorders such as Parkinson's disease and schizophrenia.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Mild tail pinch administered to rats several times daily in the presence of sweetened mild induced immediate hyperphagia and led to considerable gain in body weight. Parallels are drawn with stress-induced hyperhagia and altered affective states in obese humans.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Mild-tail-pinch induces a syndrome of eating, gnawing and licking behavior in rats in the presence of food. Detailed behavioral, pharmacological and biochemical analyses of this phenomenon resulted in the following conclusions. (1) This is an unusually reliable phenomenon, demonstrable in each of more than 200 animals tested. (2) Eating is by far the predominant response to tail-pinch. (3) Tail-pinch behavior is critically dependent on the nigrostriatal dopamine system. (4) There are striking pharmacological parallels between tail-pinch behavior and schizophrenia.
Mild tail pinch reliably and rapidly induced eating, gnawing, or licking behavior in all animals tested. Eating was by far the predominant response. Pharmacological analysis of the involvement of the brain catecholamines in tail-pinch behavior suggests that it is critically dependent on the nigrostriatal dopamine system.
Electrolytic lesions of the hypothalamic medial forebrain bundle (MFB) produced substantial deficits in the copulatory behavior of male rats, but no changes in testicular, seminal vesicle, ventral prostate or penis weights. Radioimmunoassay of serum from lesioned and control animals revealed a small but statistically insignificant reduction in testosterone and LH levels, and no change in FSH levels of lesioned males. In a second experiment, androgen levels were maintained in castrated males by subcutaneous implants of silastic capsules containing crystalline testosterone; this procedure failed to prevent the copulatory deficit which accompanied subsequent MFB lesions. We have concluded that the behavioral deficit produced by such lesions is not a direct result of pituitary-gonadal dysfunction.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.