Ethanol-induced changes in neuron and astrocyte number in the rat cerebral cortex.
Guo-qiang Zhao, Yilan Hu, Chen Peng, Shen ZhiPeng
Abstract
Guo-qiang Zhao, Yilan Hu, Chen Peng, Shen ZhiPeng
Abstract
Chronic consumption of ethanol can alter brain morphology and function. The present study examined the effect of ethanol abuse on the number of neurons and astrocytes in the rat cerebral cortex. After 45 days of ethanol treatment (2 g/kg by intraperitoneal injection), tissue samples from the rat motor cortex were Nissl-stained and probed for glial fibrillary acidic protein (GFAP) expression. The number of neurons and GFAP-immunoreactive astrocytes in each cortical layer were counted per unit area. The results showed that ethanol-treated rats had fewer neurons (P < 0.01) but a greater number of GFAP-positive astrocytes in all cortical layers as compared to control- treated animals (P < 0.01). Neuronal loss was the most pronounced in layers III and V, the major output layers of the cortex, corresponding to increased astrocyte density in these layers. These results provide evidence that chronic ethanol exposure induces neuronal death but stimulates astrocyte hyperplasia in the cerebral cortex, especially in the output layers. Loss of neurons may lead to damage to neural circuitry, while astrocyte proliferation likely serves a protective function to compensate for the resultant dysfunction of the nervous system.
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Chronic consumption of ethanol can alter brain morphology and function. The present study examined the effect of ethanol abuse on the number of neurons and astrocytes in the rat cerebral cortex. After 45 days of ethanol treatment (2 g/kg by intraperitoneal injection), tissue samples from the rat motor cortex were Nissl-stained and probed for glial fibrillary acidic protein (GFAP) expression. The number of neurons and GFAP-immunoreactive astrocytes in each cortical layer were counted per unit area. The results showed that ethanol-treated rats had fewer neurons (P < 0.01) but a greater number of GFAP-positive astrocytes in all cortical layers as compared to control- treated animals (P < 0.01). Neuronal loss was the most pronounced in layers III and V, the major output layers of the cortex, corresponding to increased astrocyte density in these layers. These results provide evidence that chronic ethanol exposure induces neuronal death but stimulates astrocyte hyperplasia in the cerebral cortex, especially in the output layers. Loss of neurons may lead to damage to neural circuitry, while astrocyte proliferation likely serves a protective function to compensate for the resultant dysfunction of the nervous system.
Key concepts: Astrocyte, Glial fibrillary acidic protein, Cerebral cortex, Nissl body, Neuron, Cortex (anatomy), Neuroscience, Central nervous system