Neuronal firing patterns, which are crucial for determining the nature of encoded information, have been widely studied; however, the molecular identity and cellular mechanisms of spike-frequency adaptation are still not fully understood. Here we show that spike-frequency adaptation in thalamocortical (TC) neurons is mediated by the Ca2+ -activated Cl- channel (CACC) anoctamin-2 (ANO2). Knockdown of ANO2 in TC neurons results in significantly reduced spike-frequency adaptation along with increased tonic spiking. Moreover, thalamus-specific knockdown of ANO2 increases visceral pain responses. These results indicate that ANO2 contributes to reductions in spike generation in highly activated TC neurons and thereby restricts persistent information transmission.
Bibliographical noteFunding Information:
This research was supported by the National Research Foundation (NRF-2014R1A2A2A01006940, NRF2015R1A3A2066619 and NRF-2014M3A7 B4051596), funded by the government of the Republic of Korea (Ministry of Science, ICT and Future Planning, MSIP), International Collaborative R&D Program, funded by the Ministry of Trade, Industry and Energy (MOTIE, Korea), the Yonsei University Future-Leading Research Initiative of 2015 (2015-22-0163), KIST Institutional Program (2E26664), Samsung Research Funding Center of Samsung Electronics under Project Number SRFC-IT1402-08 and the Brain Korea 21 (BK21) PLUS program. G.E.H., H.K., G.-E.C. and J.H. are fellowship awardee by the BK21 PLUS program.
© The Author(s) 2016.
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)
- Physics and Astronomy(all)