| First Author | Li JT | Year | 2017 |
| Journal | Cell Rep | Volume | 21 |
| Issue | 4 | Pages | 891-900 |
| PubMed ID | 29069596 | Mgi Jnum | J:254872 |
| Mgi Id | MGI:6103992 | Doi | 10.1016/j.celrep.2017.10.006 |
| Citation | Li JT, et al. (2017) Suppressed Calbindin Levels in Hippocampal Excitatory Neurons Mediate Stress-Induced Memory Loss. Cell Rep 21(4):891-900 |
| abstractText | Calbindin modulates intracellular Ca(2+) dynamics and synaptic plasticity. Reduction of hippocampal calbindin levels has been implicated in early-life stress-related cognitive disorders, but it remains unclear how calbindin in distinct populations of hippocampal neurons contributes to stress-induced memory loss. Here we report that early-life stress suppressed calbindin levels in CA1 and dentate gyrus (DG) neurons, and calbindin knockdown in adult CA1 or DG excitatory neurons mimicked early-life stress-induced memory loss. In contrast, calbindin knockdown in CA1 interneurons preserved long-term memory even after an acute stress challenge. These results indicate that the dysregulation of calbindin in hippocampal excitatory, but not inhibitory, neurons conveys susceptibility to stress-induced memory deficits. Moreover, calbindin levels were downregulated by early-life stress through the corticotropin-releasing hormone receptor 1-nectin3 pathway, which in turn reduced inositol monophosphatase levels. Our findings highlight calbindin as a molecular target of early-life stress and an essential substrate for memory. |
