| First Author | Liu Y | Year | 2016 |
| Journal | Exp Neurol | Volume | 275 Pt 1 |
| Pages | 126-32 | PubMed ID | 26476179 |
| Mgi Jnum | J:229555 | Mgi Id | MGI:5752436 |
| Doi | 10.1016/j.expneurol.2015.10.002 | Citation | Liu Y, et al. (2016) Thidoredxin-2 overexpression fails to rescue chronic high calorie diet induced hippocampal dysfunction. Exp Neurol 275 Pt 1:126-32 |
| abstractText | A high calorie diet (HCD) can impair hippocampal synaptic plasticity and cognitive function in animal models. Mitochondrial thioredoxin 2 (TRX-2) is critical for maintaining intracellular redox status, but whether it can protect against HCD-induced impairment of synaptic plasticity is unknown. We found that levels of TRX-2 are reduced in the hippocampus of wild type mice maintained for 8 months on a HCD, and that the mice on the HCD exhibit impaired hippocampal synaptic plasticity (long-term potentiation at CA1 synapses) and cognitive function (novel object recognition). Transgenic mice overexpressing human TRX-2 (hTRX-2) exhibit increased resistance to diquat-induced oxidative stress in peripheral tissues. However, neither the HCD nor hTRX-2 overexpression affected levels of lipid peroxidation products (F2 isoprostanes) in the hippocampus, and hTRX-2 transgenic mice were not protected against the adverse effects of the HCD on hippocampal synaptic plasticity and cognitive function. Our findings indicate that TRX-2 overexpression does not mitigate adverse effects of a HCD on synaptic plasticity, and also suggest that oxidative stress may not be a pivotal factor in the impairment of synaptic plasticity and cognitive function caused by HCDs. |
