Effect of prenatal exposure to ethanol on the ultrastructure of layer V of mature rat somatosensory cortex
- 1 December 1989
- journal article
- research article
- Published by Springer Nature in Journal of Neurocytology
- Vol. 18 (6) , 711-729
- https://doi.org/10.1007/bf01187226
Abstract
Recent data have shown that the structure and function of layer V pyramidal neurons, e.g. corticospinal neurons, is altered by prenatal exposure to ethanol. We examined the effect of ethanol on the ultrastructure of layer V in somatosensory cortex. Timed pregnant rats were fed a diet containing 6.7% (v/v) ethanol (E) or pair-fed a nutritionally matched control diet (C). Thirty-day-old offspring of these mothers were prepared by standard electron microscopic techniques. The somata of pyramidal and local circuit neurons and the neuropil were analysed. Prenatal exposure to ethanol induced alterations in the somata of both populations of neurons. The parallel stacking of cisternae characteristic of C-treated rats was disorganized in E-treated rats. Moreover, the Golgi complex and lysosomes occupied a larger fraction of the somata of E-treated rats. The number and frequency of symmetric axosomatic synapses, but not asymmetric axosomatic synapses, formed by both types of neurons were significantly greater in E-treated rats. Gesta tional exposure to ethanol produced a variety of changes in the neuropil. Dendrites, particularly dendritic shafts, occupied less space in E-treated rats. In contrast, axons accounted for significantly more of the neuropil in E-treated rats than in controls. This increase in axonal space was due to a significantly greater coverage by non-myelinated axons and a significantly smaller coverage by myelinated axons in E-treated rats than in C-treated rats. Although the overall frequency of synapses was similar in both treatment groups, there were significantly more asymmetric synapses in E-treated rats, and most of these were axospinous synapses. These differences may contribute to documented physiological changes such as the lower rate of glucose utilization in layer V of somatosensory cortex of E-treated rats and they may underlie the mental retardation which is characteristic of children with foetal alcohol syndrome.This publication has 54 references indexed in Scilit:
- Influence of ethanol on neuronal and synaptic maturation in the central nervous system—Morphological investigationsProgress in Neurobiology, 1988
- Maternal ethanol consumption: Lack of effect on synaptogenesis in layer I of the motor cortex in 19-day-old rat offspringExperimental Neurology, 1986
- FETAL ALCOHOL SYNDROME IS NOW LEADING CAUSE OF MENTAL RETARDATIONThe Lancet, 1986
- Ultrastructural Investigation into the Influence of Ethanol on Synaptic Maturation in Rat NeocortexDevelopmental Neuroscience, 1985
- The emergence of a discretely distributed pattern of corticospinal projection neuronsDevelopmental Brain Research, 1984
- Glycoproteins and proteins in an axolemma‐enriched fraction and myelin from developing rats: Effect of maternal ethanol consumptionJournal of Neuroscience Research, 1984
- The motor cortex of the rat: Cytoarchitecture and microstimulation mappingJournal of Comparative Neurology, 1982
- The bilaminar and banded distribution of the callosal terminals in the posterior neocortex of the ratBrain Research, 1979
- Locating corticospinal neurons by retrograde axonal transport of horseradish peroxidaseExperimental Neurology, 1977
- The effect of ethanol chronically administered to preweanling rats on cerebellar development: A morphological studyBrain Research, 1977