Long-term effects of prenatal alcohol exposure on the size of the whisker representation in juvenile and adult rat barrel cortex

Abstract

Children of mothers who abused alcohol during pregnancy are often reported to suffer from growth retardation and central nervous system (CNS) abnormalities. The use of prenatal alcohol exposed (PAE) animal models has revealed reductions in body and brain weights as well as regional specific brain deficits in neonatal pups. Recently, we and others reported reductions in the size of the posteromedial barrel subfield (PMBSF) in first somatosensory cortex (SI) associated with the representation of the large mystacial vibrissae in neonatal rats and mice that were exposed to alcohol at various times during gestation. While these reductions in barrel field size were reported in neonates, it was unclear whether similar reductions persisted later in life or whether some catch-up might take place in older animals. In the present study, we examined the effect of PAE on measures of barrel field size in juvenile (6 weeks of age) and adult (7 months of age) rats; body and brain weights were also measured. Pregnant rats (Sprague-Dawley) were intragastrically gavaged during gestational days 1-20 with alcohol (6 g/kg) to simulate a binge-like pattern of alcohol consumption (Alc); 6 g/kg alcohol produced blood alcohol levels ranging between 207.4 and 478.6 mg/dl. Chow-fed (CF), pair-fed (PF), and cross-foster (XF) groups served as normal, nutritional/stress, and maternal controls, respectively, for juvenile rats; an XF group was not included for adult rats. The major findings in the present study are (i) PAE significantly reduced the size of the total barrel field in Alc juvenile rats (13%) and adult rats (9%) compared to CF controls, (ii) PAE significantly reduced the total averaged sizes of individual PMBSF barrels in juvenile (14%) and adult (13%) rats, (iii) PAE did not significantly alter the septal area between barrels or the barrel pattern, (iv) PAE significantly reduced body weight of juvenile rats but only in comparison to PF controls (18%), (v) PAE significantly reduced whole brain (8%) and forebrain (7%) weights of juvenile rats but not adult rats, (vi) no differences were observed in forebrain/PMBSF body ratios nor was forebrain weight correlated with PMBSF area, and (vii) PAE resulted in a greater reduction in anterior barrels compared to posterior barrels. These results suggest that the effects of PAE previously reported in neonate PMBSF areas persist into adulthood.

Early postnatal alcohol exposure reduced the size of vibrissal barrel field in rat somatosensory cortex (SI) but did not disrupt barrel field organization

“…The increase in alcohol-treated group was significantly less than in GC and SC groups, which is in agreement with the results of similar studies (Thomas et al, 2003;Tomlinson et al, 1998;Tran et al, 2000). In contrast, other investigators have reported no significant weight loss in rats exposed to alcohol during early postnatal period (Chen et al, 1999;Chen et al, 1998). The significant weight reduction in alcohol-treated pups in the current study might not be due solely to alcohol exposure, but rather to combined effects of alcohol and method of feeding.…”

“…The observed significant reductions in the weights of whole brain, forebrain, and hemispheres are consistent with the findings in previous studies in which rodents were exposed to alcohol during the early postnatal period Chen et al, 1999;Chen et al, 1998;Miller, 1996;Moore et al, 2003). In addition to reductions in whole brain and hemisphere weights, the hippocampus and cerebellum are also vulnerable to alcohol exposure from P4 to P12 (Miller, 1996).…”

Diffusion MRI of the developing cerebral cortical gray matter can be used to detect abnormalities in tissue microstructure associated with fetal ethanol exposure

“…This suggests the microstructural differences observed with diffusion MRI may be persistent rather than transient with CNS development, and this is further supported by histological evidence of long-term effects of prenatal alcohol exposure on cell numbers in the rat (Chappel et al 2007). However, as others have shown in rodents (Bockhorst et al 2008, Huang et al 2008, Larvaron et al 2007, Mori et al 2001, Sizonenko et al 2007, see also Calabrese and Johnson 2013) and we and others have shown in other species (deIpolyi et al 2005, Kroenke et al 2007, 2009, McKinstry et al 2002, reviewed in Leigland and Kroenke 2011) cerebral cortical FA decreases toward an asymptotically low value during the early postnatal period (corresponding to the second half of gestation in humans; Leigland and Kroenke 2011).…”

Role of neurotrophins on postnatal neurogenesis in the thalamus: prenatal exposure to ethanol

“…The numbers of neurons in the mature brainstem and cortex are permanently reduced by prenatal exposure to ethanol (e.g., Miller and Muller, 1989; Miller and Potempa, 1990; Miller, 1995; 1999; Mooney and Miller 2007c). This is mirrored by reductions in the cortical representations in the somatosensory map (e.g., Margret et al, 2005; Powrozek and Zhou, 2005; Chappell et al, 2007). In contrast, prenatal ethanol exposure does not alter the number of neurons in the somatosensory thalamus, i.e., the ventrobasal nucleus (VB; Mooney and Miller, 1999; 2010).…”