SCIMONELLI TERESA NIEVES
Congresos y reuniones científicas
Título:
Alpha-melanocyte stimulating hormone (alpha-MSH) increase fear memory expression through melanocortin 4 receptor (MC4R)
Autor/es:
HERRERA GUADALUPE; GONZALEZ PATRICIA; MACHADO IVANA; LASAGA MERCEDES; SCIMONELLI TERESA
Lugar:
Mar del Plata
Reunión:
Congreso; XXX Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias (SAN); 2015
Institución organizadora:
Sociedad Argentina de Investigación en Neurociencias (SAN)
Resumen:

Melanocortins have important effects at central nervous system. In particular, alpha-melanocyte stimulating hormone (a-MSH) through melanocortin 4 receptor (MC4R) mediates antipyretic and neuroprotective actions. Although it has not been concretely demonstrated it has been suggest that a-MSH also could modulate learning and memory processes. We previously establish that a-MSH prevents the amnesia induced by inflammatory conditions Moreover it has been report that in vivo application of MC4R agonists increases long term potentiation in mouse hippocampal CA1 region. In addition, the activation of postsynaptic MC4R augments the number of mature dendritic spines and enhances surface expression of AMPA receptor subunit GluA1. These findings indicate that MC4R plays acritical role in the regulation of structural and functional plasticity in the hippocampus. However, the effect of a-MSH on memory consolidation has not been clearly elucidated. In the present work, we show that intrahippocampal injection of a high dose (0,5ug per side) of a-MSH after contextual fear conditioning produce a significant increase of freezing levels compare with control group indicating that the neuropeptide would be a positive modulator of memory consolidation. Conversely, the lowest doses (0,05 ug or 0,1 ug per side) did not produce changes on freezing percentage respect control group. Treatment with HS014, a specific MC4R antagonist, prevents the effect of the high dose of a-MSH on fear conditioning suggesting that a-MSH increases fear memory expression through this receptor. Western blot analysis demonstrated that fear conditioning produce ERK2 activation, a MAPK critically involved in memory consolidation, 60 min after training. The a MSH administration anticipates this effect producing an increase in pERK2 levels 15 min after conditioning in dorsal hippocampus. a-MSH and MCR4 seem to be important modulators of cognitive processes and therefore could be promising targets for pharmacological intervention in several conditions.