کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5893867 | 1568390 | 2015 | 6 صفحه PDF | دانلود رایگان |
• We studied dendritic spines of pyramidal neurons after early exposure to alcohol.
• The spine density of the apical dendrite was permanently reduced.
• Spatial distribution of spines was similar in alcohol-treated animals and controls.
• The cognitive defects of FASD may be related to the apical spine anomalies.
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.
Journal: International Journal of Developmental Neuroscience - Volume 41, April 2015, Pages 74–79