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

TAGLIAFERRO PATRICIA; DUHALDE VEGA, MAITE; EVRARD, SERGIO; RAMOS, ALBERTO J; BRUSCO, ALICIA

. Buenos Aires, Argentina

Congreso; SATELLITE MEETING OF THE INTERNATIONAL SOCIETY FOR NEUROCHEMISTRY AND AMERICAN SOCIETY FOR NEUROCHEMISTRY: Cellular and molecular mechanisms of drugs of abuse: cocaine, GHB, ibogaine and substituted amphetamines; 2001

Alcohol abuse and dependence are serious health problems throughout the world. Some reports indicate that ethanol exposure can result in neuronal damage. Astrocytes are morphological and functionally related to the neurons and astrocyte-neuron interactions provide strategic sites for actions of many chemical compounds. The aim of the present work was to study the morphological alterations of glial cells and neurons on the hippocampus after a long-term exposure using GFAP and S-100b protein and neurofilaments of 200 kDa (Nf200) immunohistochemical staining. Adult Wistar male rats (200-250 g) were exposed orally to ethanol (6.6% v/v ad libitum) during 6 weeks. Control rats received water ad libitum. After that, rats were anaesthetized and perfused with 4% paraformaldehyde in phosphate buffer 0.1M, pH 7.4. Brains were cut sagitally in 40 mm thick sections in an Oxford vibratome. Then they were processed by immunocytochemistry using anti-GFAP, anti-S-100b and anti-Nf200 antibodies. After the ethanol exposure we observed in the CA1 area of hippocampus: i) an important astroglial reaction evidenced by the presence of GFAP+ reactive astrocyte; ii) an increase in the S-100b immunostaining in the astroglial cells; and iii) a decrease in the Nf200 immunoreactivity. All these observations were confirmed by image analysis. The increased astrocytic cell area evidenced the hypertrophy of astrocytes, and the lower immunoreactivity to Nf200 was confirmed by the minor suface covered by Nf200. The increase in the S-100b immunostaining was measured as an increase in the optical density of the astroglial cells. The present study provides evidence that a long-term ethanol exposure induces alterations on the neuronal cytoskeleton and an astroglial reaction, which is a common response to brain injury and might promote functional recovery of nervous system, for example by the release of glial derived trophic factors (like S-100b) that promote cell survival and neurite growth.