NEURONAL AND ASTROGLIAL RESPONSE TO A LONG ABSTINENCE PERIOD AFTER A LOW, CHRONIC ETHANOL EXPOSURE IN THE ADOLESCENT RAT

MIROCHNIC,S; EVRARD, SG; DUHALDE VEGA, M; TAGLIAFERRO, AP; CALTANA, L; BRUSCO, A

Madison, Wisconsin , USA

Congreso; ASN 36Th Annual Meeting; 2005

Chronic ethanol (EtOH) exposure (CEE) alters neurons and glia function. Long after the cessation of a low CEE we studied some morphological parameters of neurons and astrocytes. Adolescent male Wistar rats were exposed to EtOH 6.6% v/v in drinking water for 6 weeks and studied after ending exposure or after a 10-week recovery period drinking water. Brain sections were immunostained using antibodies to gliofibrillary acidic protein (GFAP, the main cytoskeletal astrocytic protein); S-100b (a cytosolic astocytic protein secreted under 5-HT1A receptor stimulation); microtubule associated protein-2 (MAP-2, expressed mainly in dendrites); 200 kDa neurofilaments (Nf-200); neuronal nitric oxide synthase (nNOS) and serotonin (5-HT). We studied by image analysis three cognitive-related prosencephalic areas (CA1 hippocampal area, striatum and frontal cortex) and the mesencephalic dorsal and median raphe nucleus (DRN; MRN). In all the prosencephalic areas astrocytic cell area (GFAP+-cells) was increased after exposure and tended to return to normality after abstinence; the immunoreactivity (-ir) of S100b protein, the relative area of MAP-2+- and Nf-200+-fibers were decreased, and later partially recovered. In the striatum and frontal cortex nNOS-ir was decreased after abstinence. 5-HT-ir was decreased in the DRN and recovered after abstinence and was not changed in the MRN. In conclusion: to stop drinking can partially ameliorate EtOH-induced morphological changes in neurons and astroglia but cannot fully return them to the basal state. In the recovery, astrocytes may play a role and S-100b may be involved. Grant UBACYT M-072.