Juvenile separation stress induces rapid region- and layer-specific changes in S100ß- and glial fibrillary acidic protein–immunoreactivity in astrocytes of the rodent medial prefrontal cortex

The impact of juvenile stress exposure on astrocyte plasticity was assessed in the precocious rodent Octodon degus. Astrocytes expressing S100ß and glial fibrillary acidic protein (GFAP) were quantified in the limbic medial prefrontal cortex (mPFC), including the anterior cingulate (ACd), precentral medial (PrCm), infra- (IL) and prelimbic (PL) cortex and in the “non-limbic” somatosensory cortex (SSC). At the age of 21 days we compared (i) controls (C), (ii) stressed animals (SSR: separation stress/short reunion), which were exposed to 6 h separation from the family, followed by 1 h reunion with the family and (iii) stressed animals (SER: separation stress/extended reunion), which were stressed like group SSR but exposed to 48 h reunion. The observed glia response was already measurable 7 h after the onset of the stress exposure. Compared to controls SER and SSR animals showed elevated densities of S100ß-IR astrocytes in layers II/III and V–VI of the ACd, IL and PrCm, whereas no significant group differences were observed in the PL and SSC. The SSR group showed significantly decreased density of GFAP-immunoreactive astrocytes in all mPFC subregions. Only in the ACd the stress-induced changes in glia density were still evident after 48 h reunion with the family. Compared to controls, the length of GFAP-IR processes and the number of ramification points were significantly reduced in all mPFC subregions and in the SSC of the SSR group. In the SSC the stress-evoked changes in GFAP-glia density were opposite compared to the changes seen in the medial prefrontal cortical subregions, whereas the changes in GFAP-labeled processes were comparable to those observed in the mPFC. In summary, these results demonstrate that a single stress episode induces rapid and quite complex region- and cell-specific changes in glial cells, reflected by an upregulation of cytoplasmic (S100ß) and downregulation of cytoskeletal (GFAP) glial protein.