title: Ibotenic acid lesion of the hypothalamic paraventricular nucleus produces weight gain but modifies neither preference nor aversion for saccharin.
abstract: We showed recently that bilateral ibotenic acid lesions of the lateral hypothalamus (LH) produced three main behavioral disturbances in the rat, i.e., an increase in the gustatory preference and aversion thresholds for saccharin, permanent body weight and water intake deficits, and an alteration of morphine-induced modulation of taste. The two first results could suggest that the modification of the gustatory thresholds and the ingestive deficits are closely interrelated. Given this situation, we hypothesized that, conversely, a brain lesion known to induce obesity and hyperdipsia would therefore decrease the gustatory preference and aversion thresholds for saccharin. In order to test this hypothesis we analyzed the effects of the bilateral lesion of the hypothalamic paraventricular nucleus (PVH) by injection of ibotenic acid (2 micrograms in each side) on saccharin preference. The main results are as follows: 1) The neurotoxin selectively destroyed parvicellular neurons while the magnocellular cells were spared. 2) In comparison to the normal daily gain in body weight of the sham-lesioned animals, the lesioned rats showed an enhanced weight gain that became significant from the third day after the surgery up until the day of sacrifice, 37 days later. 3) In contrast to electrolytic lesions of the PVH, the ibotenic acid lesions of this nucleus did not induce hyperdipsia. 4) Preference and aversion thresholds for saccharin were not significantly modified by the lesion. 5) Whereas low doses of morphine suppressed the preference for saccharin in sham-lesioned rats when the concentration of the sweetener solution was at the threshold value, this suppressive effect was not observed in PVH-lesioned rats.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Laboratoire de Neurosciences comportementales et cognitives, URA CNRS 339-Université de Bordeaux I, Talence, France.
authors.forename: K
authors.initials: K
authors.lastname: Touzani
authors.forename: L
authors.initials: L
authors.lastname: Velley
mesh_terms: D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects* / Q000502:physiology; D001931:Brain Mapping; D003214:Conditioning, Classical / Q000187:drug effects* / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004326:Drinking / Q000187:drug effects / Q000502:physiology; D007051:Ibotenic Acid / Q000494:pharmacology*; D008297:Male; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012439:Saccharin; D012684:Sensory Thresholds / Q000187:drug effects / Q000502:physiology; D013649:Taste / Q000187:drug effects* / Q000502:physiology; D014868:Water Deprivation / Q000502:physiology; D015430:Weight Gain / Q000187:drug effects* / Q000502:physiology
chemical_list: D007051:Ibotenic Acid; D009270:Naloxone; D009020:Morphine; D012439:Saccharin