| First Author | Thibault O | Year | 2012 |
| Journal | Biochim Biophys Acta | Volume | 1822 |
| Issue | 4 | Pages | 546-9 |
| PubMed ID | 22265986 | Mgi Jnum | J:182539 |
| Mgi Id | MGI:5315815 | Doi | 10.1016/j.bbadis.2012.01.004 |
| Citation | Thibault O, et al. (2012) Reduction in neuronal L-type calcium channel activity in a double knock-in mouse model of Alzheimer's disease. Biochim Biophys Acta 1822(4):546-9 |
| abstractText | 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. |
