摘要

The alpha 7 nicotinic acetylcholine receptor (nAChR) is involved in higher cognitive and memory functions, and is associated with the etiology of neurological diseases involving cognitive decline, including Alzheimer%26apos;s disease (AD). We hypothesized that spine changes in the alpha 7 knockout might help to explain the behavioral deficits observed in alpha 7 knockout mice and prodromal hippocampal changes in AD. We quantified several measures of dendritic morphology in the CA1 region of the mouse hippocampus in Golgi-stained material from wildtype and alpha 7 knockout mice at P24. The most significant difference was a 64% increase in thin (L-type) dendritic spines on the CA1 basilar tree in knockout mice (p %26lt; .05). There were small decreases in the number of in N-type (-15%), M-type (-14%) and D-type (-4%) spine densities. The CA1 basilar dendritic tree of knockout mice had significantly less branching in the regions near the soma in comparison with wildtype animals (p %26lt; .01), but not in the more distal branching. Changes in the configuration of CA1 basilar dendritic spines have been observed in a number of experimental paradigms, suggesting that basilar dendritic spines are highly plastic. One component of cognitive dysfunction may be through alpha 7-modulated GABAergic interneurons synapsing on CA1 basal dendrites.

  • 出版日期2013-3-13