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Biochim Biophys Acta. 2012 Apr;1822(4):546-9. doi: 10.1016/j.bbadis.2012.01.004. Epub 2012 Jan 10.

Reduction in neuronal L-type calcium channel activity in a double knock-in mouse model of Alzheimer's disease.

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Department of Molecular and Biomedical Pharmacology, University of Kentucky College of Medicine, Lexington, KY 40536, USA.


Increased function of neuronal L-type voltage-sensitive Ca(2+) channels (L-VSCCs) is strongly linked to impaired memory and altered hippocampal synaptic plasticity in aged rats. However, no studies have directly assessed L-VSCC function in any of the common mouse models of Alzheimer's disease where neurologic deficits are typically more robust. Here, we used cell-attached patch-clamp recording techniques to measure L-VSCC activity in CA1 pyramidal neurons of partially dissociated hippocampal "zipper" slices prepared from 14-month-old wild-type mice and memory-impaired APP/PS1 double knock-in mice. Surprisingly, the functional channel density of L-VSCCs was significantly reduced in the APP/PS1 group. No differences in voltage dependency and unitary conductance of L-VSCCs were observed. The results suggest that mechanisms for Ca(2+) dysregulation can differ substantially between animal models of normal aging and models of pathological aging.

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