ALCOHOL EXPOSURE DURING ADULTHOOD INDUCES NEURONAL AND ASTROGLIAL ALTERATIONS ON THE HIPPOCAMPAL CA1 AREA.

TAGLIAFERRO P.; DUHALDE VEGA, M; EVRARD S.; RAMOS, AJ; BRUSCO, A

ANNALS OF THE NEW YORK ACADEMY OF SCIENCES.

Año: 2002 vol. 965 p. 334 - 342

0077-8923

Ethanol (ETOH) exposure can result in neuronal damage. Astrocytes are morphologic and functionally related to neurons, and astrocyteneuron interactions provide strategic sites for the actions of many chemical compounds. The aim of the present work was to study the morphologic alterations of glial cells and neurons on the hippocampus after long-term ETOH exposure using GFAP and S-100b protein, neurofilaments of 200 kDa (Nf200), MAP2, and serotonin transporter (5HT-T) immunocytochemical staining. Adult Wistar male rats (200–250 g) were orally exposed to ETOH (6.6% v/v ad libitum) for 6 weeks. Control rats received water ad libitum. Brain sections from control and exposed rats were processed by immunocytochemistry. After ETOH exposure we observed in the CA1 area of the hippocampus: (1) an important astroglial reaction evidenced by the presence of GFAP+ reactive astrocytes; (2) an increase in S-100b immunostaining in astroglial cells; and (3) a decrease in Nf200, 5HT-T, and MAP2 immunoreactivity. The current study provides evidence that long-term ETOH exposure induces alterations in the neuronal cytoskeleton and an astroglial reaction, which is a common response to brain injury and may promote functional recovery of the nervous system, as by the release of glial-derived trophic factors (such as S-100â) that promote cell survival and neurite growth.