Early postnatal exposure to alcohol reduces the number of neurons in the occipital but not the parietal cortex of the rat.

Background: The rat brain undergoes a period of rapid growth in the early postnatal period. During this time, the neocortex seems to be vulnerable to ethanol injury. Subdivisions of the neocortex develop in a temporospatial gradient that is likely to determine their vulnerability to ethanol-induced damage and whether damage is permanent. Therefore, the authors investigated the effect of postnatal ethanol exposure on the neocortex and specific subregions at the cessation of exposure and in the mature brain.

Methods: Four-day-old rat pups with intragastric cannulae were artificially reared from postnatal day (PN) 4 through PN9. Of 12 daily feeds, two consecutive feeds contained either ethanol (4.5 g/kg) or an isocaloric maltose/dextrin solution. On PN10 or PN115, animals were perfused intracardially, and the brains were removed. Stereological methods were used to determine the total number of neurons and glial cells in, and the volume of, the neocortex, the parietal cortex, and the occipital cortex.

Results: Exposure to ethanol did not affect body or brain weight at PN10. In contrast, at PN115 forebrain weight was significantly lower in ethanol-exposed animals compared with control-treated animals. There was no effect of treatment on body weight at PN115. On PN10, neocortical volume was 15% smaller in the ethanol-exposed animals compared with controls, with no change in the total number of neurons or glial cells. Occipital cortical volume was reduced by 22% in the ethanol-exposed animals, with a significant deficit in the total number of neurons (ethanol-exposed, 2.62 x 10; gastrostomy control, 3.20 x 10). There was no effect of ethanol exposure on the total number of glial cells in the occipital cortex or on any parameter in the parietal cortex. There was also no significant effect of ethanol exposure on the occipital cortex on PN115.

Conclusions: These findings provide support for the hypothesis that a specific area or cell population might be differentially vulnerable to ethanol exposure during the brain growth spurt and that cell deficits evident on PN10 may not be permanent.