060 | Aging alters biochemical and molecular basis of memory, in the rat temporal cortex.


Author: Nicolas Andres Deyurka | Email: nadeyurka@unsl.edu.ar

Nicolas Andres Deyurka , Maria Gabriela Lacoste , Ana Cecilia Anzulovich

1° Laboratorio de Cronobiología (LABCRON), IMIBIO-SL, CONICET-UNSL.
2° Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis.

Aging is a progressive, accumulative and deleterious process occurring in most living species. The temporal cortex (TC) is one of the neocortical association areas that underlies the long-term storage of declarative memory and it is particularly affected by aging. Here, we studied how aging affects the biochemical and molecular basis of memory, in the TC of male Holtzman rats. For this purpose, we analyzed BMAL1 and RORa protein levels, Bdnf, Rc3 and Nrf2 mRNA levels, CAT and GPx expression and enzymatic activity, and lipid peroxidation levels, in the TC of 3- and 22-mo-old rats. An IBM SPSS Box-Plot analysis showed no variation in BMAL1 and RORa protein levels nor CAT antioxidant activity, decreased GPx expression and activity (p<0.01 and p<0.01, respectively) and Nrf2 mRNA levels (p<0.05), and increased MDA levels (p<0.05), in the TC of aged animals. However, unexpectedly, Bdnf and Rc3 mRNA levels increase significantly, with the aging process (p<0.0001 and p<0.01). Previously, we observed that aging abolishes circadian rhythms of clock transcription factors, BMAL1 and RORa, in the TC. This may produce an internal desynchronization between metabolism and antioxidant defenses, increasing the oxidative stress. Thus, the resulting oxidative redox environment would alter the endogenous clock activity and clock-controlled genes expression such as Cat, Gpx, Bdnf and Rc3. Increased expression of Bdnf and Rc3 would be important to maintain cortical functions in the aged animals.