| First Author | Konsolaki E | Year | 2015 |
| Journal | Cereb Cortex | Volume | 25 |
| Issue | 8 | Pages | 2138-48 |
| PubMed ID | 24554727 | Mgi Jnum | J:234229 |
| Mgi Id | MGI:5789511 | Doi | 10.1093/cercor/bhu019 |
| Citation | Konsolaki E, et al. (2015) Premature Aging Phenotype in Mice Lacking High-Affinity Nicotinic Receptors: Region-Specific Changes in Layer V Pyramidal Cell Morphology. Cereb Cortex 25(8):2138-48 |
| abstractText | The mechanisms by which aging leads to alterations in brain structure and cognitive deficits are unclear. Alpha deficient cholinergic system has been implicated as one of the main factors that could confer a heightened vulnerability to the aging process, and mice lacking high-affinity nicotinic receptors (beta2(-/-)) have been proposed as an animal model of accelerated cognitive aging. To date, however, age-related changes in neuronal microanatomy have not been studied in these mice. In the present study, we examine the neuronal structure of yellow fluorescent protein (YFP(+)) layer V neurons in 2 cytoarchitectonically distinct cortical regions in wild-type (WT) and beta2(-/-) animals. We find that (1) substantial morphological differences exist between YFP(+) cells of the anterior cingulate cortex (ACC) and primary visual cortex (V1), in both genotypes; (2) in WT animals, ACC cells are more susceptible to aging compared with cells in V1; and (3) beta2 deletion is associated with a regionally and temporally specific increase in vulnerability to aging. ACC cells exhibit a prematurely aged phenotype already at 4-6 months, whereas V1 cells are spared in adulthood but strongly affected in old animals. Collectively, our data reveal region-specific synergistic effects of aging and genotype and suggest distinct vulnerabilities in V1 and ACC neurons. |
