Effects of lateral hypothalamic lesions on the anorexia induced by ethanolamine-O-sulfate

Intracisternal (IC) injection of the GABA-transaminase inhibitor, ethanolamine-O-sulfate (EOS), has been previously shown to induce dose-dependent anorexia in normal rats as well as to reverse overeating in several rodent models of acute and chronic hyperphagia. To determine if such anorexia might be mediated by cells within or fibers of passage which traverse the lateral hypothalamus (LH), adult female rats received bilateral radiofrequency heat lesions of the LH vs. anesthesia control injections and were allowed to recover normal feeding and drinking responses. Using a longitudinal design, all animals then received 100, 0, and 200 micrograms EOS in 20 microliters deionized water IC with 1 week separating each injection. In addition to daily measures of feeding, drinking and body weight, all animals were screened 24 hr after injections for sensorimotor competence and general health by testing open-field activity, catalepsy, paw-lick responses on a hot-plate and rectal temperature. As reported previously, IC EOS induced dose-dependent hypophagia and weight loss. However, the magnitude and duration of these effects were equivalent in lesioned and control rats. In addition, open-field activity and body temperature were reliably lowered as a function of dosage while catalepsy was increased. Again, this effect was equivalent in lesioned and control rats. Subsequent tests of drinking and feeding in response to hyperosmotic and hypoglycemic challenges, respectively, confirmed that lesioned rats were deficient compared to controls. These findings suggest that an intact LH axis is not required for the anorexigenic effects of IC EOS.