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Numbers of neurons and glia in mature rat somatosensory cortex: Effects of prenatal exposure to ethanol
Author(s) -
Miller Michael W.,
Potempa Gregory
Publication year - 1990
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.902930108
Subject(s) - neuropil , somatosensory system , biology , endocrinology , stereology , medicine , cresyl violet , liquid diet , neuroglia , anatomy , cortex (anatomy) , ethanol , central nervous system , neuroscience , biochemistry , staining , genetics
Stereological methods were used to examine the consequences of prenatal exposure to ethanol on the structure of area 3, primary somatosensory cortex, of the mature hooded rat. Pregnant rats were fed a liquid diet containing 6.7% (v/v) ethanol (Et), pairfed an isocaloric liquid control diet (Ct), or fed a diet of chow and water (Ch). Cresyl violet‐stained sections of 3‐month‐old pups were examined. The corrected mean size of the cell bodies of neurons in layers other than layer V was significantly smaller in the Ettreated rats; conversely, the mean somatic size of glia in each layer was significantly larger in the Ettreated rats. The laminar cell packing density for neurons and glia, however, was similar in rats from both treatment groups. The overall volume of area 3 and the volume of individual layers were about 33% smaller in Et‐treated rats than in the pair‐fed controls. Thus, the estimated total number of neurons in Et‐treated rats (1.79*10 6 ) was significantly fewer than in Chtreated rats (2.77*10 6 ) and in Ct‐treated rats (2.66*10 6 ). The total number of glia also was about 30% fewer in Et‐treated rats than in the controls. Not all layers were affected equivalently. The space occupied by the neuropil was significantly greater in Et‐treated rats, but only in layers II/III, IV, and VI; hence, the cell body/neuropil ratio in these layers was less in Et‐treated rats than in the controls. Therefore, microcephaly caused by prenatal exposure to ethanol results not only from a miniaturization of the brain, but also from a permanent abnormal organization of cerebral cortex.