Astroglial and cognitive effects of chronic cerebral hypoperfusion in the rat.

The permanent occlusion of common carotid arteries (2VO) causes a significant reduction of cerebral blood flow (hypoperfusion) in rats and constitutes a well established experimental model to investigate neuronal damage and cognitive impairment that occurs in human ageing and Alzheimer's disease. In the present study, we evaluated two astroglial proteins--S100B and glial fibrillary acidic protein (GFAP)--in cerebral cortex and hippocampus tissue, glutamate uptake and glutamine synthetase activity in hippocampus tissue, as well as S100B in cerebrospinal fluid. Cognition, as assessed by reference and working spatial memory protocols, was also investigated.

S100B levels in the cerebrospinal fluid of rats are sex and anaesthetic dependent.

1. S100B is a calcium-binding protein that acts as a neurotrophic cytokine and is expressed in the central nervous system, predominantly by astrocytes. At nanomolar concentrations, S100B stimulates neurite outgrowth and glial glutamate uptake, as well as protecting neurons against glutamate excitoxicity.

Hippocampal antioxidant system in neonates from methylmercury-intoxicated rats.

Methylmercury (MeHg) is a well-known environmental pollutant toxic to the nervous tissue, particularly during development. We recently described transitory hippocampal changes in neonate rats prenatally exposed to MeHg. In this study, we evaluate oxidative stress in the hippocampus on the 1st and 30th postnatal days.

Cerebrospinal fluid S100B increases reversibly in neonates of methyl mercury-intoxicated pregnant rats.

Methylmercury (MeHg), an organic methylated form of mercury, is one of the most hazardous environmental pollutants. MeHg is a potent neurotoxin, particularly during brain development. Neurotoxicity-induced by MeHg in prenatal age can cause mental disorders, cerebral palsy and seizures.