Neocortical neurodegeneration in young adult Wistar rats prenatally exposed to ethanol

• Published in: Neurotoxicology and teratology Vol. 28; no. 2; pp. 229 - 237
• Main Authors: Fakoya, Francis Adelade, Caxton-Martins, Ezekiel Ademola
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.03.2006; Elsevier Science
• Subjects: Age Factors; Alcoholism and acute alcohol poisoning; Animals; Animals, Newborn; Apoptosis; Biological and medical sciences; Birth Weight - drug effects; Body Weight - drug effects; Cell Count - methods; Ethanol - toxicity; Female; Gestational Age; Immunohistochemistry - methods; In Situ Nick-End Labeling - methods; Male; Medical sciences; Neocortex; Neocortex - drug effects; Neocortex - pathology; Neurodegeneration; Neurodegenerative Diseases - chemically induced; Neurodegenerative Diseases - pathology; Neuronal count; Organ Size - drug effects; Pregnancy; Prenatal ethanol exposure; Prenatal Exposure Delayed Effects; Pyramidal Cells - drug effects; Pyramidal Cells - metabolism; Pyramidal Cells - pathology; Random Allocation; Rats; Rats, Wistar; Toxicology; Wistar rats; Wistar rats; Neocortex; Neurodegeneration; Prenatal ethanol exposure; Apoptosis; Neuronal count; Human; Ethanol; Rat; Rodentia; Exposure; Numeration; Prenatal; Alcoholic beverage; Vertebrata; Mammalia; Neuron; Cell death; Young adult; Adult animal
• ISSN: 0892-0362; 1872-9738
• DOI: 10.1016/j.ntt.2005.11.001

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 μm thickness stained for neurohistology from each group. Another set of specimens was cryosectioned at − 23 °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.