Essential Role for TRPC5 in Amygdala Function and Fear-Related Behavior

Antonio Riccio, Yan Li, Jisook Moon, Kwang Soo Kim, Kiersten S. Smith, Uwe Rudolph, Svetlana Gapon, Gui Lan Yao, Evgeny Tsvetkov, Scott J. Rodig, Ashlee Van't Veer, Edward G. Meloni, William A. Carlezon, Vadim Y. Bolshakov, David E. Clapham

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)761-772
Number of pages12
Issue number4
StatePublished - May 15 2009
Externally publishedYes



ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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