Long-term effects of early life deprivation on brain glia in Fischer rats.

Abstract:

:Both clinical and experimental studies have indicated that depression and depression-like animal conditions are associated with disruption of the intrinsic plasticity of the brain, resulting in neuronal atrophy. However, little is known about the brain glia in these conditions. Early life stress in the form of infant abuse or neglect constitutes a risk factor in the aetiology of major depressive disorder in later life. It is possible to model this relation between early life stress and depression in the rat through maternal deprivation; in adulthood, this postnatal manipulation is known to lead to depression-like behaviour. In the stress-hyperresponsive Fischer strain, P1-14 pups were isolated for 4 h/day (early deprivation, ED, n=6) or were nonhandled (NH, n=6); they were left undisturbed until adulthood. Postmortem quantitative analysis of regional astroglial distribution and morphology based on glial fibrillary acidic protein (GFAP) immunohistochemistry indicated a significant effect of ED on the density of GFAP-reactive astrocytes in brain areas implicated in stress-related behaviour. A moderate (10-22%) but consistent reduction in GFAP-reactive astrocyte density was seen in dorsal dentate gyrus, prefrontal cortex, ventral hippocampal CA1, cingulate cortex, dorsal hippocampal CA1 and basolateral amygdala. The ED-related reduction in GFAP-immunoreactive astrocyte density was more marked than the reduction in total cell density, which suggests that GFAP immunoreactivity, rather than the number of astrocytes, was reduced. This study provides evidence that early life stress leads to long-term changes in the density of astroglia in the brain regions involved in stress responses in the rat.

journal_name

Brain Res

journal_title

Brain research

authors

Leventopoulos M,Rüedi-Bettschen D,Knuesel I,Feldon J,Pryce CR,Opacka-Juffry J

doi

10.1016/j.brainres.2007.01.039

subject

Has Abstract

pub_date

2007-04-20 00:00:00

pages

119-26

eissn

0006-8993

issn

1872-6240

pii

S0006-8993(07)00135-7

journal_volume

1142

pub_type

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