EVIDENCES OF A NEUROPROTECTIVE ROLE OF BUSPIRONE IN PRENATAL ETHANOL EXPOSURE

EVRARD, SG; DUHALDE VEGA, M; RAMOS, AJ; TAGLIAFERRO,AP; RUBIO, MD; BRUSCO, A

New Orleans, USA

Congreso; SFN 33rd Annual Meeting; 2003

Prenatal ethanol exposure (PEE) is the cause of fetal alcohol syndrome. Serotonergic system and astrocytes are impaired by PEE. After the stimulation of its 5HT1A receptors, astrocytes release the S100b protein, an astroglial neurotrophic factor that has developmental and neuroplastic actions. PEE also affects the glial fibrillary acidic protein (GFAP) expression. We postnatally studied in PEE rat offspring the possible neuroprotective action of a prenatal treatment with buspirone, a 5HT1A agonist. Serotonin (5HT), 5HT transporter (5HTT), GFAP and intracellular S100b expression were studied. Female Wistar rats were exposed to ethanol 6.6% (v/v) in drinking water for 6 weeks before breeding and during gestation; control groups received water. Pregnant rats were divided into four treatment groups: CS (control-saline), CB (control-buspirone), ES (ethanol-saline) and EB (ethanol-buspirone). Between E13 and E20 each group received a daily subcutaneous dose (4.5 mg/kg) of buspirone or an equivalent volume of saline. Ethanol was discontinued at P0. On P5, P21, P35, P60 and P90, pup’s brains were processed by immunocytochemistry using antibodies directed to 5HT, 5HTT, GFAP or S100b. Relative area of 5HTT+ fibers, cell area of GFAP+ astrocytes and relative optical density of 5HT+ neurons and S100b+ astrocytes were measured by computer-assisted image analysis. The results showed significant differences for all the markers in ES group but not in CS, CB and EB at different ages. Thus, we showed a normalization of the measured parameters when buspirone was prenatally administered to PEE rats. Then, buspirone may have a neuroprotective role in PEE.