Increases in Programmed Death and Degenerative Changes to Neurons in the Mesocorticolimbic Dopaminergic System as a Possible Cause of Congenital Alcohol Dependence

• Published in: Neuroscience and behavioral physiology 2013, Vol.43 (1), p.10-16
• Main Authors: Droblenkov, A. V., Karelina, N. R.
• Format: Article
• Language: English
• Subjects: Addictive behaviors; Alcoholism; Animals; Apoptosis; Behavior; Behavioral Sciences; Biomedical and Life Sciences; Biomedicine; Brain; Dopamine; Ethanol; Females; Morphology; Neurobiology; Neurons; Neurosciences; Pathogenesis
• ISSN: 0097-0549; 1573-899X
• DOI: 10.1007/s11055-012-9684-x

Congenital alcohol dependence (CAD) is known to be based on insufficiency of the mesocorticolimbic dopaminergic system (MDS). The lack of data on the numbers and volumes of MDS cell bodies and the rate of their programmed death in the offspring of alcoholized humans and animals hinders our understanding of the pathogenesis of CAD. Morphological changes to neurons and in the numbers of macrogliocytes in the main areas of the MDS were studied in the offspring of intact Wistar rats ( n = 20) and rats consuming 15% ethanol solution for five months, including the periods of mating and pregnancy ( n = 20). Specimens were collected on days 0, 5, 10, and 61. Sections stained by the Nissl method and for glial fibrillary acidic protein were used to determine the proportions of unaltered, hypochromic, pyknomorphic, and ghost neurons, the volumes of unaltered neurons, the numbers of oligodendrocytes and astrocytes, and the glial-neuronal index. On day 61 of life, there were significant reductions in the numbers of unaltered and slightly altered MDS neurons due to increases in programmed neuron death (apoptosis) and cell shrinkage, combined with partial compensatory increases in the extent of neuron-glial interactions (due to oligodendrocytes); alcohol motivation was present in these animals.