This study tested the hypothesis that prenatal ethanol exposure during the
last third of gestation, including the brain growth spurt (BGS), in the gui
nea pig produces neurobehavioural teratogenicity, manifesting as brain grow
th restriction and hyperactivity. Pregnant guinea pigs (term, about gestati
onal day (GD) 68) received oral administration of ethanol (2 g/kg maternal
body weight per day on GD 43 and/or GD 44 and then 4 g/kg maternal body wei
ght per day from GD 45 to GD 62), isocaloric-sucrose/pair-feeding, or water
. Maternal blood ethanol concentration (BEC) on GD 57 or 58, at 1 h after t
he daily dose, was 340 +/- 76 mg/dl (n = 8). Ethanol treatment decreased br
ain, cerebral cortical, hippocampal, and cerebellar weights at GD 63 (P <0.
05), and decreased brain and cerebral cortical weights at postnatal day 10
(P <0.05), with no effect on body weight and no apparent effect on spontane
ous locomotor activity. The data demonstrate that, in the guinea pig, prena
tal ethanol exposure during the last third of gestation, including the BGS,
decreases brain weight that persists into postnatal life, which is associa
ted with growth restriction of the cerebral cortex. However, this prenatal
ethanol exposure regimen, including the BGS, does not increase spontaneous
locomotor activity in contrast to the persistent hyperactivity that occurs
after chronic ethanol exposure throughout gestation. (C) 2001 Elsevier Scie
nce Inc. All rights reserved.