Feeding induced by pharmacological blockade of fatty acid metabolism is selectively attenuated by hindbrain injections of the galanin receptor antagonist, M40.
Galanin has been shown to stimulate feeding when injected intracranially in rats. Lesion and Fos studies have shown that the neural pathway for feeding stimulated by mercaptoacetate (MA)- induced blockade of fatty acid oxidation includes several structures rich in galanin cell bodies or terminals. In the present experiment, we examined the role of hindbrain galanin in feeding stimulated by MA. We found that galanin (1 nmol) stimulates feeding when injected in the nucleus of the solitary tract (NTS), a site that is crucial for MA-induced feeding, or into the fourth ventricle (4V, 1 or 5 nmol) and that NTS or 4V injections of the galanin receptor antagonist, M40 (1.5 or 5 nmol), completely blocked feeding induced by MA (68 mg/kg). The effect of the M40 appeared to be specific for MA-induced feeding, since M40 did not significantly attenuate either feeding induced by the antimetabolic glucose analog, 2-deoxy-D-glucose (2DG, 100 or 200 mg/kg), or deprivation-induced water intake. Results suggest that feeding induced by decreased fatty acid oxidation relies upon galaninergic terminals in the hindbrain. Furthermore, results indicate that hindbrain neurons involved in MA-induced feeding differ neurochemically from those important for 2DG-induced feeding.[1]References
- Feeding induced by pharmacological blockade of fatty acid metabolism is selectively attenuated by hindbrain injections of the galanin receptor antagonist, M40. Koegler, F.H., Ritter, S. Obes. Res. (1996) [Pubmed]
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