Abstract

Dendritic spines are the main postsynaptic sites of excitatory connections of neocortical pyramidal neurons. Alterations of spine shape, number, and density can be observed in different mental diseases, including those caused by developmental alcohol exposure. Pyramidal neurons of layer 2/3 are the most abundant cells of the neocortex and represent the main source of associative cortico-cortical connections. These neurons are essential for higher functions mediated by the cortex such as feature selection and perceptual grouping. Furthermore, their connections have been shown to be altered in experimental models of fetal alcohol spectrum disorders.Here, we used a Golgi-like tracing method to study the spine density of layer 2/3 associative pyramidal neurons in the somatosensory cortex of adult rats exposed to alcohol during the first postnatal week.The main result of the present study is represented by the decreased spine density in the apical dendrite of alcohol-treated rats, as compared to controls. As to the basal dendritic tree, there were no significant differences between the experimental and the control group.A decreased density of dendritic spines in the apical dendrite may impair the excitatory input onto pyramidal neurons, thus resulting in a widespread alteration of the cortical information flow.

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