doi:10.1016/j.brainres.2005.11.024
Copyright © 2005 Elsevier B.V. All rights reserved.
Research Report
Altered organization of cortical interneurons in rats exposed to ethanol during neonatal life
Alberto Granato
, 
Department of Psychology, Catholic University, L.go A. Gemelli 1-20123 Milan, Italy
Accepted 2 November 2005.
Available online 28 December 2005.
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Abstract
The fetal alcohol syndrome (FAS) is a known cause of mental retardation in humans. Studies based on experimental models of FAS have demonstrated deep alterations of the cerebral cortex. Here, the anatomical organization of cortical interneurons immunoreactive for different calcium binding proteins has been studied in adult rats exposed to alcohol inhalation during the first week of postnatal life. The main finding is represented by an increase of calretinin neurons in ethanol-treated animals compared to controls and by a corresponding decrease of calbindin neurons. The radial distribution of these neurons was also modified in ethanol-treated cases. These changes were evident both in the primary motor and somatosensory area. No significant differences were found in the number and distribution of parvalbumin interneurons. The functional implications of these data and their significance for FAS are discussed.
Keywords: Calbindin; Calretinin; Parvalbumin; Fetal alcohol syndrome; GABA; Mental retardation
Neuroscience classification codes: Development and regeneration, Cerebral cortex and limbic system
Abbreviations: ANOVA, analysis of variance; BAC, blood alcohol concentration; C, control cases; CaBPs, calcium binding proteins; CB, calbindin-D-28K; CR, calretinin; Et, ethanol-treated cases; FAS, fetal alcohol syndrome; M1, primary motor cortex; N, normally reared animals; PV, parvalbumin; S1, primary somatosensory cortex
Fig. 1. Microphotographs showing the morphological features of immunoreactive elements in ethanol-treated cases. (A) Calbindin neurons in layer 5 of S1. (B) Calretinin neurons in layer 2/3 of S1. (C) Parvalbumin neurons in layer 5 of M1. Note the labeled terminals surrounding immunonegative pyramidal neurons. Scale bar = 40 μm.
Fig. 2. (A, B) Microphotographs showing calbindin immunoreactivity in M1 of a control (A) and an ethanol-treated case (B). (C, D) Microphotographs showing calbindin immunoreactivity in S1 of a control (C) and an ethanol-treated case (D). Scale bar = 100 μm.
Fig. 3. Bar graphs showing the mean number of CB, CR, and PV immunoreactive neurons in M1 and S1 of normally reared (N), control (C), and ethanol-treated (Et) cases. T bars represent standard deviations. *P < 0.05. **P < 0.01. The post hoc comparisons, carried out by means of the Tukey test, showed that, both for CB and CR, N and C animals represent homogeneous subsets, as opposed to Et cases.
Fig. 4. (A, B) Microphotographs showing calretinin immunoreactivity in M1 of a control (A) and an ethanol-treated case (B). (C, D) Microphotographs showing calretinin immunoreactivity in S1 of a control (C) and an ethanol-treated case (D). Scale bar = 100 μm.
Fig. 5. (A, B) Microphotographs showing parvalbumin immunoreactivity in M1 of a control (A) and an ethanol-treated case (B). (C, D) Microphotographs showing parvalbumin immunoreactivity in S1 of a control (C) and an ethanol-treated case (D). Scale bar = 100 μm.
Table 1.
Mean and standard deviation of the estimated volumes of M1 and S1 in N, C, and Et animals

Differences between groups were not significant (F2,9 = 0.31 for M1; 0.45 for S1).