ABSTRACT
Alcohol induces impairment of cognition, learning and memory. Neurotoxic effects of alcohol on the pathology of the hippocampus and the cingulate cortex were investigated in experimental rats. Parvalbumin (PV), a calcium-binding protein, is a crucial component of GABAergic neurons and glial fibrillary acidic protein immunoreactive (GFAP-ir) astrocytes have been used as markers. We investigated the effects of ethanol exposure during adulthood on the PV-ir neurons and GFAP-ir astrocytes in the hippocampus and the cingulate cortex of 3-month-old male Wistar rats. The rats were divided into 2 groups: control (C) and alcohol-exposed groups. The control group received distilled water whereas the alcohol-exposed groups received either a low dose (20%w/v, LD) or high dose (40%w/v, HD) of ethanol for periods of 21 days, 3 or 6 months. The brains of the animals were processed for immunohistochemistry using anti-parvalbumin and anti-GFAP antibodies and the numbers of PV immunoreactive (PV-ir) neurons and GFAP-ir astrocytes were counted/unit area. For each period of administration, the number of PV-ir neurons was significantly reduced for groups exposed to both the low and the high doses of ethanol compared to those of control groups in both the hippocampus and the cingulate cortex (p<0.01). In addition, the number of PV-ir neurons was progressively reduced after prolonged ethanol exposure. In contrast, there was a significantly increased number of GFAP-ir astrocytes observed in the hippocampus and the cingulate cortex in all groups exposed to ethanol and this was a function of both the duration and the dose of ethanol exposure, indicating that PV-ir neurons are as sensitive as the GFAP-ir astrocytes to ethanol exposure. Our data indicate that alcohol exposure induced a reduction of PV-ir neurons and an increase of GFAP-ir astrocytes in the hippocampus and the cingulate cortex and this may be associated with the impairment of cognition, learning and memory after chronic alcohol administration.