Maternal ethanol consumption and synaptic membrane glycoproteins in offspring

Abstract

The present study was undertaken to assess the influences of chronic maternal ethanol consumption, prior to and during gestation, on the development of synaptic plasma membranes (SPMs) and on the synthesis of SPM glycoproteins in offspring. Comparisons were made between animals whose mothers were pair-fed a control or 6.6% (v/v) ethanol liquid diet in which protein accounted for either 18% (original) (C & E) or 21% (revised) (*C & *E) of the calories. In addition, groups of pups that were either cross-fostered (*C & *E) with chow-fed surrogate mothers or reverse cross-fostered (offspring of chow-fed mothers with *C & *E mothers) were examined. Ethanol and matched (same dietary group) control pups had comparable brain and body weights, brain protein content, and yield of SPM proteins during the 10-24 day age period examined. However, the yield of SPM proteins from ethanol and control offspring of and/or reared by the three groups of rat mothers that received the *E and *C liquid diets was greater than that of the offspring of rats that were fed the original diets. This suggests that the original diets were not nutritionally adequate for pregnant rats. Despite the fact that the content of SPM proteins was comparable in ethanol and matched control pups, the offspring of ethanol-treated rats had an abnormal distribution of [3H]- or [14C]-fucose-derived radioactivity among SPM glycoproteins. The SPM abnormalities were most severe in the non-cross-fostered offspring of E rats. No SPM glycoprotein abnormalities were found in the reverse cross-fostered group. The results of the present study demonstrate that chronic maternal ethanol consumption prior to parturition has a severe effect on the synthesis of SPM glycoproteins in developing offspring without affecting the content of SPMs per se. It also demonstrates the importance of optimizing the composition of liquid diets used to feed pregnant rats.

Disialotransferrin developmental deficiency syndrome.

“…The well known neuronal cell and tract impairments caused by alcohol are of certain interest in this connection. 8 The reason for the changes in the sialic acid transferrin pattern in alcoholics is unknown but there is some evidence that ethanol may inhibit glycosylation of glycoproteins with derangement of the carbohydrate composition of the glycoproteins, transferrin in particular.9 It would not be unreasonable to suspect that the disialotransferrindevelopmental deficiency syndrome described in this study might as regards clinical manifestations be the effect of similar mechanisms, perhaps representing an inborn error of metabolism.…”

In Utero Ethanol Exposure Increases Proenkephalin, a Precursor of a Neuropeptide That Is Inhibitory to Neuronal Growth

“…The liquid diets are administered for 6 weeks before breeding and during gestation (Noronha and Druse, 1982). Ethanol replaces a portion of carbohydrate in the control diet and accounts for 35% of the calories.…”

Glycoproteins and proteins in an axolemma‐enriched fraction and myelin from developing rats: Effect of maternal ethanol consumption

“…These studies have provided anatomical and biochemical evidence [Barnes and Walker, 1981;Hammer and Scheibel, 1981;Sherwin et al, 1981;West et al, 1981;Noronha and Druse, 1982;StibIer et al, 19831 that neuronal and synaptic development are impaired in the offspring of ethanol-treated female animals. There is also evidence of CNS myelin abnormalities Malone, 1976, 1979;Druse and Hofteig, 1977;Jacobson et al, 1979;Lancaster et al, 19821.…”

“…Numerous studies of animal models of the fetal alcohol syndromeieffects (FAS/ FAE) have been undertaken in an attempt to provide an explanation for the neural abnormalities found in the offspring of alcoholic women [see Clarren and Smith, 1978, for a review of FAS] . These studies have provided anatomical and biochemical evidence [Barnes and Walker, 1981;Hammer and Scheibel, 1981;Sherwin et al, 1981;West et al, 1981;Noronha and Druse, 1982;StibIer et al, 19831 that neuronal and synaptic development are impaired in the offspring of ethanol-treated female animals. There is also evidence of CNS myelin abnormalities Malone, 1976, 1979;Druse and Hofteig, 1977;Jacobson et al, 1979;Lancaster et al, 19821. However, there is a conflict as to whether or not maternal alcohol consumption results in a delay of CNS myelination and myelin maturation in offspring.…”