117 | Acute intrahippocampal administration of melanin-concentrating hormone (MCH) impairs memory consolidation and decreases the expression of MCHR-1 and TrkB receptors

Cognition, Behavior, and Memory

Author: PATRICIA LAGOS | Email: plagos@fmed.edu.uy

Vicente Ruiz-Viroga , Marialuisa De Ceglia , Laura Morelli , Eduardo M. Castaño , Eduardo Blanco-Calvo , Juan Suárez , Fernando Rodríguez de Fonseca , Pablo Galeano , Patricia Lagos

1° Unidad Académica de Fisiología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay
2° UGC Salud Mental, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Universidad de Málaga, Málaga, Spain.
3° Laboratory of Brain Aging and Neurodegeneration, Fundación Instituto Leloir (IIBBA-CONICET), Ciudad Autónoma de Buenos Aires, Argentina
4° IBIMA, Departamento de Psicobiología y Metodología de las Ciencias del Comportamiento, Universidad de Málaga, Málaga, Spain.

Melanin-concentrating hormone (MCH) is a hypothalamic neuropeptide with a role in memory processes. Our study seeks to provide new evidences about its participation in memory consolidation and its relation with glutamatergic and BDNF/TrkB system. MCH (25, 50, 200, and 500 ng) was acutely administered in both hippocampi of male rats immediately after finishing the sample trial of two hippocampal-dependent behavioral tasks: the Novel Object Recognition Test (NORT) and the modified Elevated Plus Maze test. Results indicated that MCH (200 and 500 ng) impaired memory consolidation in both tasks compared with vehicle-treated rats. A second group of experiments were performed with MCH 200 ng, administered alone or co-administered with a MCHR-1 antagonist (ATC-0175) at the end of the sample trial in the NORT. After that, the hippocampi were dissected out to study the expression of MCHR-1, BDNF, TrkB and NMDA subunits. The co-administration of MCH (200 ng) with ATC-0175 reverted the MCH-dependent detrimental effect on memory. Moreover, MCH induced a significant decrease in MCHR-1 and TrkB expression but did not modify BDNF and NMDA receptor subunits NR1, NR2A, and NR2B expression. These results suggest that MCH in vivo elicits pro-amnesic effects in the rat hippocampus by decreasing the availability of its receptors and TrkB receptors, thus linking both endogenous systems to memory processes. Further experiments will be performed in order to explore such interesting connection.