Enriched environment prevents the hippocampal synaptic alterations observed in middle-aged rats that suffered perinatal asphyxia

GALEANO, PABLO; BLANCO CALVO, EDUARDO; ROMERO, JUAN IGNACIO; LOGICA TORNATORE, TAMARA; UEHARA, JUAN MARTÍN; CAPANI, FRANCISCO

Buenos Aires

Exposici�n; II Congreso Argentino de Microscopía; 2012

Asociación Argentina de Microscopía (SAMIC)

Perinatal asphyxia remains as one of the most important causes of death and disability in children, without an effective treatment [1]. We have previously found hippocampal-dependent memory deficits in young adult [2] and middle-aged rats (unpublished results), which had undergone acute birth asphyxia. On the other hand, exposure to enriched environment has been shown to be beneficial in different models of brain injury [3]. The main aim of the present study was to assess if perinatal asphyxia worsens some of the synaptic alterations frequently observed in middle-aged rats. As well as, if life-long exposure to an enriched environment could prevent those alterations. To this end, rats born vaginally (CTL), by cesarean section (C+), or by cesarean section following 19 min of asphyxia (PA) were assigned to enriched (EE) or standard environment (SE) at 21 days of age, for 18 months. The SE consists of stainless steel cages of 29 cm × 21 cm × 34 cm (2 animals in each cage). The EE consists of large cages of 100 cm × 50 cm × 50 cm (6 animals in each cage) furnished with a large cord pending from the top of the cage, two inclined rambles, suspended bridges, PVC cylinders and 3 running wheels. The four walls of each cage were made of interwoven metal wires allowing the animals to move in all directions. Every week, five different safe toys objects were provided to every enriched cage. Results indicated that PA rats reared in SE showed a reduced synaptic density in CA1 region of the hippocampus in comparison with CTL and C+ rats reared in the same environment. On the other hand, EE increased synaptic density in all groups, being significantly higher in CTL and C+ rats (see Fig. 1 and 2). It is concluded that life-long exposure to EE prevents the hippocampal synaptic alterations observed in middle-aged rats that had undergone acute birth asphyxia.