| First Author | Riccio A | Year | 2009 |
| Journal | Cell | Volume | 137 |
| Issue | 4 | Pages | 761-72 |
| PubMed ID | 19450521 | Mgi Jnum | J:148915 |
| Mgi Id | MGI:3847140 | Doi | 10.1016/j.cell.2009.03.039 |
| Citation | Riccio A, et al. (2009) Essential role for TRPC5 in amygdala function and fear-related behavior. Cell 137(4):761-72 |
| abstractText | The transient receptor potential channel 5 (TRPC5) is predominantly expressed in the brain where it can form heterotetrameric complexes with TRPC1 and TRPC4 channel subunits. These excitatory, nonselective cationic channels are regulated by G protein, phospholipase C-coupled receptors. Here, we show that TRPC5(-/-) mice exhibit diminished innate fear levels in response to innately aversive stimuli. Moreover, mutant mice exhibited significant reductions in responses mediated by synaptic activation of Group I metabotropic glutamate and cholecystokinin 2 receptors in neurons of the amygdala. Synaptic strength at afferent inputs to the amygdala was diminished in P10-P13 null mice. In contrast, baseline synaptic transmission, membrane excitability, and spike timing-dependent long-term potentiation at cortical and thalamic inputs to the amygdala were largely normal in older null mice. These experiments provide genetic evidence that TRPC5, activated via G protein-coupled neuronal receptors, has an essential function in innate fear. |
