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Mitochondrial function in mouse brain cortex synaptosomes during aging. Alterations in motor performance

Paulina Lombardi

  • CABA,
  • Argentina
  • Paulina Lombardi ¹
  • , Analía G Karadayian ¹
  • , Juan I. Guerra ¹
  • , Rodolfo Cutrera ³
  • , Juanita Bustamante ²
  • 1 Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Fisicoquímica, Buenos Aires, Argentina. CONICET- Universidad de Buenos Aires, Instituto de Bioquímica y Medicina Molecular (IBIMOL), Buenos Aires, Argentina
  • 2 Centro de Altos Estudios en Ciencias de la Salud, Universidad Abierta Interamericana, Buenos Aires, Argentina
  • 3 CONICET - Universidad de Buenos Aires, Instituto de Fisiología y Biofísica Bernardo Houssay, (IFIBIO), Buenos Aires, Argentina

The aging process is characterized by a progressive decline of physiological and metabolic functions. Changes in mitochondrial bioenergetics and increased free radical production have been associated with brain aging. With the purpose of analyzing the effect of aging in motor performance and mitochondrial function in nerve terminals, 3-, 10- and 20-month-old mice were used. For evaluation of motor performance, tightrope and footprint tests were carried out. Brain cortex synaptosomes were isolated by a Ficoll gradient procedure. Mitochondrial function, cardiolipin content and reactive oxygen species were determined. Behavioral results showed a decrease in neuromuscular coordination in 10 and 20-month old mice (80-70%) and impairment in gait balance in the oldest mice (increase in step distance and overlap at 70%) as compared with young animals. Likewise, preliminary results show that acetylcholinesterase activity was increased by 35% in the oldest mice. Moreover, changes were observed in enzymatic activity of mitochondrial respiratory complexes with aging. Increased superoxide levels (11 and 21%) were found in 10- and 20-month-old mice as compared with young animals. H2O2 production rates were 43% decreased in the oldest mice. Mitochondrial membrane potential and cardiolipin content were unaffected in aged mice. It seems that respiratory complexes activity and ROS modulation could contribute to preserve mitochondrial integrity and function in synaptic terminals.