<abstract xmlns="http://www.w3.org/1999/xhtml">Leptin inhibits feeding, reduces body weight and increases thermogenesis. Experimental data suggest involvement of GABAergic mechanisms in the regulation of feeding behavior and energy balance. The present study was set to determine the effect of combinations from leptin, GABAB-agonist baclofen and GABAB-antagonist CGP35348 on thermoregulation of male Wistar rats, using in vivo and in vitro experiments. The substances used for in vivo experiments were administered intraperitoneally (i.p.). The measurement of the body temperature was done via thermistor probes (TX8) and monitored on multichannel recorder Iso-Thermex16. In vitro experiments were conducted on rat PO/AH neurons, recorded extracellulary by conventional electrophysiological equipment, using brain slice preparations. The separate intraperitoneal injection of leptin as well as GABAB-antagonist CGP35348 produced significant hyperthermia in rats while the GABAB-agonist baclofen caused a decrease in the core body temperature. The probable synergy between the hyperthermic effects of leptin and GABAB-antagonist did not occur. On the contrary, the effect of this combination was lower as compared to the result of the separate administration of GABAB-antagonist. When leptin was applied just prior to GABAB-agonist baclofen, neither of their separate effects appeared. In vivo effects determined correlated with in vitro changes of firing rate observed in PO/AH neurons. The data from this study provide a new point of view concerning the interactions of leptin and GABA on the level of thermoregulation. These results represent a step forward in understanding the complicated mechanisms involved in thermoregulation.</abstract>

Leptin inhibits feeding, reduces body weight and increases thermogenesis. Experimental data suggest involvement of GABAergic mechanisms in the regulation of feeding behavior and energy balance. The present study was set to determine the effect of combinations from leptin, GABAB-agonist baclofen and GABAB-antagonist CGP35348 on thermoregulation of male Wistar rats, using in vivo and in vitro experiments. The substances used for in vivo experiments were administered intraperitoneally (i.p.). The measurement of the body temperature was done via thermistor probes (TX8) and monitored on multichannel recorder Iso-Thermex16. In vitro experiments were conducted on rat PO/AH neurons, recorded extracellulary by conventional electrophysiological equipment, using brain slice preparations. The separate intraperitoneal injection of leptin as well as GABAB-antagonist CGP35348 produced significant hyperthermia in rats while the GABAB-agonist baclofen caused a decrease in the core body temperature. The probable synergy between the hyperthermic effects of leptin and GABAB-antagonist did not occur. On the contrary, the effect of this combination was lower as compared to the result of the separate administration of GABAB-antagonist. When leptin was applied just prior to GABAB-agonist baclofen, neither of their separate effects appeared. In vivo effects determined correlated with in vitro changes of firing rate observed in PO/AH neurons. The data from this study provide a new point of view concerning the interactions of leptin and GABA on the level of thermoregulation. These results represent a step forward in understanding the complicated mechanisms involved in thermoregulation.

Leptin and Gaba Interactions on Thermoregulation of Rats

Department of Pharmacology &Toxicology, Faculty of Medicine, Medical University of Sofia

Journal of Biomedical and Clinical Research

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

{"article-title":"Leptin and Gaba Interactions on Thermoregulation of Rats"}

Leptin inhibits feeding, reduces body weight and increases thermogenesis. Experimental data suggest involvement of GABAergic mechanisms in the regulation of...

Leptin and Gaba Interactions on Thermoregulation of Rats

Publié en ligne: 10 déc. 2015

Pages: 20 - 24

DOI: https://doi.org/10.1515/jbcr-2015-0120

© 2015

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.