Abstract
The anorexic action of amphetamine is thought to be mediated by central dopaminergic and noradrenergic neurotransmitter systems1–4. However, some of its sympathomimetic effects can be attenuated by denervation5 or by depletion of peripheral noradrenaline6,7. This led us to consider the possibility that a component of amphetamine anorexia might be due to excitation of the sympathetic innervation of the viscera. To test this, the amphetamine dose–response curves of free-feeding rats with visceral sympathetic denervation by coeliac ganglionectomy (GAN) were compared with those of sham-operated controls (SHM). We report here that ganglionectomized rats were protected from the anorexic effects of low doses of amphetamine (0.2 or 0.4 mg per kg interaperitoneal, i.p.). We suggest that the anorexia might result from enhanced hepatic glycogenolysis8, and the subsequent stimulation of hepatic metabolic receptors that inhibit feeding9.
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Tordoff, M., Hopfenbeck, J., Butcher, L. et al. A peripheral locus for amphetamine anorexia. Nature 297, 148–150 (1982). https://doi.org/10.1038/297148a0
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DOI: https://doi.org/10.1038/297148a0
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