Neocortical neurodegeneration in young adult Wistar rats prenatally exposed to ethanol.

This study was aimed to determine the persistence of neurodegeneration in the cerebral cortex of adult Wistar rats following prenatal ethanol exposure. Timed pregnant rats maintained on standard mouse chow (Ladokun Feeds, Ibadan, Nigeria) and water ad libitum were used for the study. The rats were divided randomly into groups A and B (n-6) and C (n = 4). Group A received a daily ethanol dose of 5.8 g/Kg body weight/day, on the 9th, 10th, 11th, and 12th days of gestation by intragastric intubation, at 16.00 h (PEE) group B was pair-fed with the ethanol dams on isocaloric solution of sucrose for the same duration (PF), while group C received standard chow (C) and water ad libitum. At birth, the pups were weighed and weaned at 30 days of age. Wet brain weights of adult offsprings were determined at 42 days of age. Following whole body perfusion-fixation after anaesthesia, specimens of the neocortex were processed routinely for paraffin embedding and sections of 6 mum thickness stained for neurohistology from each group. Another set of specimens was cryosectioned at -23 degrees C and evaluated for apoptosis by the TUNEL method. The study showed a significantly sustained 44% reduction in brain weight. Neurodegeneration was evident in the layer V, consisting of mostly pyknotic pyramidal neurons, with broken dendrites, collapsed cell bodies, obliterated nuclei and nucleoli. There was a 55% decrease in the normal pyramidal neuron cell pack density. The negative TUNEL signals in both groups suggest that apoptosis may play no role in the mechanism of action occurring at this age of the animals. These sustained changes may underlie the neurobehavioural deficits that have been variously reported.

Morphological alterations in the seminiferous tubules of adult Wistar rats: the effects of prenatal ethanol exposure.

This study presents the effects of prenatal ethanol exposure on the morphology of the seminiferous tubules of the testes in the adult male rat. Timed-pregnant adult female Wistar rats (average weight 200 g) were given daily intragastric intubation of 5.8 g/kg ethanol between gestation days 9 and 12. Pair-fed and ad lib-fed animals served as controls. The pups were weighed at birth and weaned at 30 days. At 42 days of age the male offspring (n = 10) from each group were anaesthetised and the testes removed and weighed. Another set of male rats from each group (n = 6), were anaesthetised, whole body perfused and the testes removed and processed for paraffin embedding. Sections were subjected to morphological analysis and morphometric measurements based on computerised techniques following haematoxylin and eosin, PAS and reticulin staining. The results demonstrated that prenatal ethanol exposure induced persistent growth retardation and a 66% reduction in testicular weight and severely altered the morphology of the seminiferous tubules of adult male rats, causing a reduction in the cross-sectional area of the tubules by 18%, germinal epithelium thickness by 21% (p < 0.001) and an inhibition of spermatogenesis. The study showed the absence of reticulin fibres in the peritubular tissue of seminiferous tubules of prenatal ethanol-exposed adult male rats. The results imply that damage following prenatal ethanol exposure occurs irreversibly in utero and persists into adulthood in the exposed animals, which may have implications for male fertility.