期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2001
卷号：98
期号：5
页码：2797-2802
DOI：10.1073/pnas.051346398
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：We model experience-dependent plasticity in the cortical representation of whiskers (the barrel cortex) in normal adult rats, and in adult rats that were prenatally exposed to alcohol. Prenatal exposure to alcohol (PAE) caused marked deficits in experience-dependent plasticity in a cortical barrel-column. Cortical plasticity was induced by trimming all whiskers on one side of the face except two. This manipulation produces high activity from the intact whiskers that contrasts with low activity from the cut whiskers while avoiding any nerve damage. By a computational model, we show that the evolution of neuronal responses in a single barrel-column after this sensory bias is consistent with the synaptic modifications that follow the rules of the Bienenstock, Cooper, and Munro (BCM) theory. The BCM theory postulates that a neuron possesses a moving synaptic modification threshold, {theta}M, that dictates whether the neuron's activity at any given instant will lead to strengthening or weakening of its input synapses. The current value of {theta}M changes proportionally to the square of the neuron's activity averaged over some recent past. In the model of alcohol impaired cortex, the effective {theta}M has been set to a level unattainable by the depressed levels of cortical activity leading to "impaired" synaptic plasticity that is consistent with experimental findings. Based on experimental and computational results, we discuss how elevated {theta}M may be related to (i) reduced levels of neurotransmitters modulating plasticity, (ii) abnormally low expression of N-methyl-D-aspartate receptors (NMDARs), and (iii) the membrane translocation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in adult rat cortex subjected to prenatal alcohol exposure.
