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Developmental changes in content of glial marker proteins in rats exposed to protein malnutrition
Ana Maria Feoli1, Marina C Leite, Ana Carolina Tramontina
1Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Insights
Protein malnutrition during development causes early brain inflammation (astrogliosis) in rats, with some lasting changes in cerebrospinal fluid suggesting potential long-term brain damage risks.
Area of Science:
- Neuroscience
- Developmental Biology
- Nutritional Science
Background:
- Protein malnutrition (PMN) impacts brain development.
- Glial cell responses to PMN are not well understood.
- Specific glial markers like GFAP, S100B, and GS are key indicators.
Purpose of the Study:
- To investigate glial changes in rats exposed to pre- and postnatal PMN.
- To assess GFAP, S100B, and GS in different brain regions and cerebrospinal fluid.
- To determine the impact of PMN on brain development and potential long-term effects.
Main Methods:
- Rats were subjected to pre- and postnatal protein malnutrition.
- GFAP, S100B immunocontents, and GS activity were measured.
- Analyses were conducted in the cerebral cortex, hippocampus, cerebellum, and cerebrospinal fluid at postnatal days 2, 15, and 60.
Main Results:
- Early astrogliosis (increased GFAP, S100B, GS) observed in the cerebral cortex, hippocampus, and cerebellum at birth.
- Persistent elevation of S100B in cerebrospinal fluid was noted from early stages through day 60.
- No significant long-term changes in GFAP, S100B, or GS were found in brain tissue by day 60.
Conclusions:
- PMN induces transient astrogliosis at birth, potentially mediated by ERK activation.
- The cerebral cortex shows regional vulnerability to malnutrition.
- Persistent changes in cerebrospinal fluid S100B suggest potential long-term brain damage or disease risk.
Abstract:
Pre- and postnatal protein malnutrition (PMN) adversely affects the developing brain in numerous ways, but only a few studies have investigated specific glial parameters. This study aimed to evaluate specific glial changes of rats exposed to pre and postnatal PMN, based on glial fibrillary acidic protein (GFAP) and S100B immunocontents as well as glutamine synthetase (GS), in cerebral cortex, hippocampus, cerebellum and cerebrospinal fluid, on the 2nd, 15th and 60th postnatal days. We found increases in GFAP, S100B and GS in the cerebral cortex at birth, suggesting an astrogliosis. Hippocampus and cerebellum also exhibited this profile at birth. However, a significant interaction between age and diet in postnatal life was observed only in the S100B of the cerebral cortex. No changes in the content of GFAP and S100B and GS activity were found on the 60th postnatal day in malnourished rats. In contrast, following an increase in the levels of S100B in the cerebrospinal fluid, during the early developmental stages, levels remained elevated on the 60th postnatal day. Our data support the concept of astrogliosis at birth, induced by PMN, and involve extracellular-regulated kinase activation. Specific alterations in cerebral cortex emphasize the regional vulnerability of the brain to malnutrition; some alterations were observed only at birth (e.g. GFAP); others were observed on the 2nd and 15th post-natal days (e.g. ERK phosphorylation). Taken together, transient and persistent alterations (e.g. elevated extracellular levels of S100B) suggest some brain damage or a risk of brain diseases in rats exposed to PMN.
