Deficits in short term memory following neonatal anoxia are related to the inhibitory circuitry and recovered in an enriched environment
Neonatal anoxia is the total oxygen deprivation that occurs at birth, and it is a significant contributor to neonatal morbidity and mortality, causing 24% of all neonatal deaths worldwide. In addition, the survivors can present sequels such as cerebral palsy, epilepsy, learning and memory, and cognitive deficits, an important issue in public health. The interactions between the hippocampus and prefrontal cortex (PFC) have been studied as an essential key role in various cognitive and behavioral functions. It may be affected by oxygen deprivation. The interneurons have been studied as necessary to regulate the communication between the hippocampus and PFC in cognitive functions. Our study investigated the consequences of neonatal anoxia in adult rats on memory and recognition in Barnes Maze, novel and displaced object recognition tasks. Indeed we evaluate the parvalbumin (PV) interneurons on the prefrontal cortex subdivided into infralimbic and prelimbic cortex, and hippocampus in CA1, CA3 and DG gyrus. We found an increase of PV cells in anoxia animals in CA1. The western blot analysis of vesicular GABA transporter (VGAT) and vesicular glutamate transporter 1 (VGLUT1) showed that anoxia promotes an increase in inhibitory synapses. Then, we investigate whether the environmental enrichment could recover the memory deficits in anoxia animals, which led to being beneficial. The electrophysiological recordings showed that anoxia animals had decreased beta and gamma oscillations events in exploratory behavior, and the enrichment during the development could rescue those patterns.