RESUMO
Experimental paradigms conducted to assess the neurotoxic effects of ethanol exposure on hippocampus development have yielded controversial findings. Hippocampal CA1 population and some cytoarchitectural parameters of pyramidal cells were studied after exposure to ethanol during early development, in rats. Examination of 30-day-old offspring of rats exposed to moderate levels of ethanol during gestation through lactation showed an increased volume of the hippocampal CA1 field compared to untreated or pair-fed control pups, as well as a reduced number of pyramidal neurons. In addition, the number of spines from surviving CA1 pyramidal neurons was reduced. Furthermore, stubby and wide spines were proportionally increased, while the proportion of mushroom and ramified spines was reduced; no variation in the proportion of thin spines was observed. Because alcoholic women usually drink alcohol before, during, and after pregnancy, a broad-range experimental model of alcohol exposure was used in this study. The present findings show that experimental exposure to moderate levels of ethanol, resembling the human situation in alcoholic mothers, leads to loss of hippocampal CA1 pyramidal neurons, along with several pathological and plastic events in the dendritic arborization of these neurons. Some ethanol-induced excitotoxicity-related mechanisms, which may be underlying these effects, are discussed.
Assuntos
Animais Recém-Nascidos/fisiologia , Depressores do Sistema Nervoso Central/toxicidade , Etanol/toxicidade , Hipocampo/patologia , Animais , Peso Corporal/efeitos dos fármacos , Morte Celular/efeitos dos fármacos , Feminino , Tamanho da Ninhada de Vivíparos/efeitos dos fármacos , Masculino , Plasticidade Neuronal/efeitos dos fármacos , Tamanho do Órgão/efeitos dos fármacos , Gravidez , Efeitos Tardios da Exposição Pré-Natal , Ratos , Ratos Sprague-Dawley , SobrevidaRESUMO
Migration of the external granular layer cells in the cerebellum of rats was delayed after exposure to moderate levels of ethanol during a pre-gestational period, through gestation and lactation until weaning. After ethanol withdrawal, cell soma and dendrites were observed to be larger in granule cells. Likewise, Bergmann glia showed several cytoarchitectonic features suggesting cell immaturity, as well as some apparent compensatory plastic responses after ethanol withdrawal. These effects may be due to ethanol impairing neurotrophin-mediated processes during cerebellar development that could lead to alterations in Purkinje cell structure and activity, and thereafter in the psychoneural functions in which the cerebellar cortex is involved.