Indomethacin attenuates hyperthermia produced by anterior coronal lateral hypothalamic knife cuts.

Electrolytic lesions of the lateral hypothalamus (LH) and coronal knife cuts of fibers anterior to the LH produce an elevation in core body temperature, or hyperthermia. Prostaglandin has been shown to mediate hyperthermia produced by electrolytic LH lesions. The present study characterizes the time course and the role of prostaglandin in mediating knife-cut-induced hyperthermia. Results show that the prostaglandin synthesis inhibitor indomethacin significantly attenuates hyperthermia produced by the knife cuts, suggesting that prostaglandin is involved in mediating this temperature increase. A disruption of axonal fibers that project from the LH to the preoptic area is postulated to be responsible for the temperature increase. There was no effect of knife cuts on food intake and body weight loss, which were also measured, suggesting that this fiber system is not involved in feeding behavior.

Participation of the substantia nigra dopaminergic neurons in the occurrence of gastric mucosal erosions.

Previous reports indicate that dopaminergic systems play an important role on gastric mucosal erosions. In the present study, the participation of intrinsic neurons of the substantia nigra (SN) and ventral tegmental area (VTA) on the occurrence of stomach ulceration was investigated. It was found that bilateral microinfusions of a neurotoxic dose (20 microg/microl) of N-methyl-D-aspartate (NMDA) into the SN, but not in the VTA, lead to gastric erosions 24 h after the surgery. A decrease in dopamine levels in the caudate 24 h after the microinfusion of NMDA into the SN was also observed. Destruction of SN cell bodies with 6-hydroxydopamine (6-OHDA) did not induce gastric ulceration or changes in dopamine levels in the caudate nucleus 24 h after the lesioning procedure. NMDA neurotoxicity is mediated by the acute excitatory or activational effects, in contrast to 6-OHDA, suggesting that the occurrence of gastric ulceration after the infusion of NMDA into the SN is not due to the cell death per se but is related to an overactivation of these cells that precede their death. Taken together, these results suggest that modulation of dopaminergic levels by neurons located within the SN may play an important role for the development of gastric erosions.