| First Author | Balleza-Tapia H | Year | 2018 |
| Journal | Elife | Volume | 7 |
| PubMed ID | 30417826 | Mgi Jnum | J:269412 |
| Mgi Id | MGI:6269227 | Doi | 10.7554/eLife.37703 |
| Citation | Balleza-Tapia H, et al. (2018) TrpV1 receptor activation rescues neuronal function and network gamma oscillations from Abeta-induced impairment in mouse hippocampus in vitro. Elife 7:e37703 |
| abstractText | Amyloid-beta peptide (Abeta) forms plaques in Alzheimer's disease (AD) and is responsible for early cognitive deficits in AD patients. Advancing cognitive decline is accompanied by progressive impairment of cognition-relevant EEG patterns such as gamma oscillations. The endocannabinoid anandamide, a TrpV1-receptor agonist, reverses hippocampal damage and memory impairment in rodents and protects neurons from Abeta-induced cytotoxic effects. Here, we investigate a restorative role of TrpV1-receptor activation against Abeta-induced degradation of hippocampal neuron function and gamma oscillations. We found that the TrpV1-receptor agonist capsaicin rescues Abeta-induced degradation of hippocampal gamma oscillations by reversing both the desynchronization of AP firing in CA3 pyramidal cells and the shift in excitatory/inhibitory current balance. This rescue effect is TrpV1-receptor-dependent since it was absent in TrpV1 knockout mice or in the presence of the TrpV1-receptor antagonist capsazepine. Our findings provide novel insight into the network mechanisms underlying cognitive decline in AD and suggest TrpV1 activation as a novel therapeutic target. |
