Effects Of Alcohol Exposure During Pregnancy On Dendritic Spine And Synapse Of Visual Cortex In Filial Mice

Alcohol abuse causes injuries of multiple organs and tissues affecting the brain, liver, cardiovascular system, immune system. Fetal alcohol syndrome (FAS) is a serious injury to fetus and child caused by maternal prenatal exposure. Due to their specific functions in learning and memory, the pathologic alterations of synapses and dendritc spines should be used to explain the neurobehavioral deficits after prenatal or postnatal alcohol exposure. To better understand the development of synapse and dendritic spine after prenatal alcohol exposure, we analyzed dendritic spines and synaptic ultrastucture in visual cortex of mice from P0-P30 after prenatal ethanol consumption, and the dose-dependent and long-term affecting alterations of synapse and dendritic spine were investigated in visual cortex. Pregnant mice were intubated ethanol daily from E5 through the pup's birth to establish mode of prenatal alcohol abuse. The dendritic spines of pyramidal cells in visual cortex of pups were labeled with DiI diolistic assay, and the synaptic ultrastructure was observed under transmission electron microscope. The results show: 1.Nascent synapses were seen as early as E15, although these were immature and were composed of a presumed presynaptic terminal with pleiomorphic vesicles in the vicinity of a partner cell body or projection. The postsynaptic plasmalemma remained unspecialized and the gap between pre- and postsynaptic plasmalemmas was only 5-10 nm, significantly narrower than the mature synaptic cleft. With increasing age there was gradual thickening of both the pre- and postsynaptic membranes, with widening of the synaptic cleft to 15-20 nm. Ultrastructurally mature synapses were not seen until P7; at this time both Gray's type I and II could be observed. Synapse maturation was synchronous with dendritic spine differentiation, synaptic specialization may be dependent on dendritic spine maturation and the expression of presynaptic vesicle components. In the meantime, the study also indicated that the synaptogenesis was connected with the development and maturation of neocortex. 2. Prenatal alcohol exposure could induce dendritic spines of pyramidal neurons in visual cortex to decrease in their number and elongate in their length. These changes are dose-dependent with long term effect even at postnatal 30. The ultrastructural alterations could also be found in synapse, for example, decreased synaptic vesicle, narrow synaptic cleft. The alterations of dendritic pine and synaptic ultrastructure probably were the manifestations of the retardation of visual cortical development. Their long-term effect is one of the causes of lifelong mental retardation of FAS in childhood.