Quantitative changes in reduced nicotinamide adenine dinucleotide phosphate-diaphorase-reactive neurons in the brain of Octodon degus after periodic maternal separation and early social isolation

Abstract

The influence of preweaning maternal separation and postweaning social isolation on the development of reduced nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase-reactive neurons in prefrontal cortical areas, in subdivisions of the nucleus accumbens and in the corpus callosum was quantitatively investigated in the precocious rodent Octodon degus. Forty-five-day-old degus from three animal groups were compared: (i) degus that were reared under normal undisturbed social conditions; (ii) degus that were repeatedly separated from their mothers during the first three postnatal weeks and thereafter reared with their family; and (iii) degus that remained undisturbed with the family until weaning (postnatal day 21) and thereafter were reared in social isolation. Preweaning maternal separation led to a significant decrease in NADPH-diaphorase-containing neurons in the corpus callosum in both genders (down to 33%) compared with the social control group. No significant changes were found in the subregions of the medial prefrontal cortex and nucleus accumbens. Postweaning social isolation led to a reduced density of NADPH-diaphorase-containing neurons in the corpus callosum in both genders (down to 52%) compared with the social control group. Furthermore, in the precentral medial cortex of female pups, a significant reduction in NADPH-diaphorase-reactive neurons (down to 72%) was detectable. All other regions of the medial prefrontal cortex and the nucleus accumbens remained unchanged. The observed deprivation-induced changes may reflect either an excessive reduction in NADPH-diaphorase-positive neurons or a down-regulation of the enzyme in neurons that normally express it. Our results indicate a link between early adverse socio-emotional experience and the maturation of NADPH-reactive neurons. Further studies are required to analyse the functional implications of this experience-induced brain pathology.