Effect of prenatal exposure to ethanol on the ultrastructure of layer V of mature rat somatosensory cortex

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. Gestational 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.

Selective effects of perinatal ethanol exposure in medial prefrontal cortex and nucleus accumbens

“…Using the three trimester equivalent exposure model, we demonstrate significant alterations on dendritic morphology in layer II/III mPFC pyramidal cells similar to those previously reported in the hippocampus (Abel et al, 1983, Davies and Smith, 1981, Durand et al, 1989, Gonzalez-Burgos et al, 2006, Kuge et al, 1993, Saunders et al, 1995, Tarelo Acuna et al, 2000), visual cortex (Cui et al 2010) and sensory cortex (al-Rabiai and Miller 1989, Fabregues et al, 1985, Galofre et al, 1987, Hammer and Scheibel 1981, Stoltenburg-Didinger and Spohr, 1983) following developmental ethanol exposure. This study is the first to utilize fully reconstructed neurons in the mPFC to quantify spine density and distribution following ethanol exposure during development and shows specific and localized reductions of spines on basilar and apical dendrites proximal to the cell body.…”

Long-term alterations of striatal parvalbumin interneurons in a rat model of early exposure to alcohol

“…FASD is characterized by multiple impairments such as deficit of attention and learning, language difficulties, and mnemonic and intellectual development anomalies [2]. Its genesis can be explained by the deep structural and functional alterations of cortical neurons [3,4]. Serious motor impairments have also been described [5] and can be partly explained by the altered functional organization of the motor cortex [6,7].…”

Chromatin Switches during Neural Cell Differentiation and Their Dysregulation by Prenatal Alcohol Exposure

“…Additionally, prenatal alcohol exposure alters the distribution and morphology of neurons [101,129]. Ectopic distribution and density of neuronal synapses generated late in gestation have been reported [116,130,131,132,133,134]. …”