The nature of encoded information in neural circuits is determined by neuronal firing patterns and frequencies. This paper discusses the molecular identity and cellular mechanisms of spike-frequency adaptation in the central nervous system (CNS). Spike-frequency adaptation in thalamocortical (TC) and CA1 hippocampal neurons is mediated by the Ca2+-activated Cl- channel (CACC) anoctamin-2 (ANO2). Knockdown of ANO2 in these neurons results in increased number of spikes, in conjunction with significantly reduced spike-frequency adaptation. No study has so far demonstrated that CACCs mediate afterhyperpolarization currents, which result in the modulation of neuronal spike patterns in the CNS. Our study therefore proposes a novel role for ANO2 in spike-frequency adaptation and transmission of information in the brain.
Bibliographical noteFunding Information:
This research was supported by the National Research Foundation (NRF-2014R1A2A2A01006940 and NRF-2014M3A7B4 051596) funded by the government of the Republic of Korea (Ministry of Science, ICT & 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), Samsung Research Funding Center of Samsung Electronics under Project Number SRFC-IT1402-08, and the Brain Korea 21 (BK21) PLUS program. GEH is fellowship awardee by BK21 PLUS program.
All Science Journal Classification (ASJC) codes
- Molecular Biology