Proceedings of The Physiological Society

Puerto de la Cruz, Tenerife (2003) J Physiol 548P, P139

Poster Communications

Antagonistic galanin-NPY interactions in food intake response: a functional and quantitative receptor autoradiography study

Zaida Díaz-Cabiale, María García-Coronel, Carmen Vela, Rosa Garrido, Margarita Remirez de Esparza, Rafael Coveñas, Salvador González-Barón and Jose Angel Narváez

Departamento de Fisiología, Facultad de Medicina, Universidad de Málaga, Málaga, Spain

The aim of this work was to investigate if galanin (GAL) could modulate the feeding responses induced by NPY in satiated rats. We have studied the possible modulation by GAL of the responses elicited by central administration of Y1 and Y2 receptor agonists and also the effect of GAL on their binding characteristics by using receptor autoradiography.

Animals were chronically canulated in the lateral ventricle under sodium pentobarbitone anaesthesia and recovered for 1 week. Food consumption was measured 60 min after intracerebroventricular injections of the Y1 agonist Leu31-Pro34-NPY (2.5 nmol) or the Y2 agonist NPY (13-36) (2.5 nmol) alone or in combination with an effective or a threshold dose of GAL (3.0 nmol and 0.1 nmol respectively). Quantitative receptor autoradiography was performed in brain slices containing the hypothalamus. 125I-labelled Leu31-Pro34-NPY (25 pM) and 125I-labelled PYY (13-36) (25 pM) were used as the Y1 and Y2 agonist, respectively, and the binding was studied in the absence or presence of GAL (1 nM). At the end of the experiments animals were humanely killed.

Feeding responses observed after central administration of the Y1 agonist were counteracted by the presence of a threshold dose of GAL (P < 0.05), but no additive effects were found in the presence of an effective dose of GAL. The responses of food intake were not modified by the coadministration of both Y2 agonist and GAL at any of the doses tested. Receptor autoradiography showed that 125I-labelled Leu31-Pro34-NPY binding decreased in the presence of GAL exclusively in the nucleus arcuatus by 30 % (P < 0.05); however, GAL was not able to modified the binding of 125I-labelled PYY (13-36) in any of the hypothalamic areas studied.

In conclusion, the functional results demonstrate that GAL antagonizes selectively the feeding responses mediated by NPY Y1 receptor subtypes and the autoradiography data show that GAL decreases exclusively the binding of Y1 agonist. These data evidence that the GAL/NPY antagonism is mediated by the modulation of Y1 receptors probably as a consequence of receptor interactions at the membrane level. This interaction may be of relevance for the understanding the modulation of central control of feeding response by neuropeptides.

This work has been supported by Spanish BFI2001-1905.

Where applicable, experiments conform with Society ethical requirements