The Ca2+-activated chloride channel anoctamin-2 mediates spike-frequencyadaptation and regulates sensory transmission in thalamocortical neurons
Autor: | Jaekwang Lee, C. Justin Lee, Jea Kwon, Go Eun Ha, Joohyeon Hong, Hee-Sup Shin, Hankyul Kwak, Eun Mi Hwang, Soon Young Jung, Gyeong Eon Chang, Eunji Cheong, Kiyeong Song |
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Jazyk: | angličtina |
Rok vydání: | 2016 |
Předmět: |
Male
0301 basic medicine Patch-Clamp Techniques Sensory Receptor Cells Science Thalamus Anoctamins General Physics and Astronomy General Biochemistry Genetics and Molecular Biology Article Adenoviridae Mice 03 medical and health sciences 0302 clinical medicine Gene Knockdown Techniques medicine Animals Humans Tonic (music) ortho-Aminobenzoates Patch clamp Bestrophins Author Correction Mice Inbred BALB C Gene knockdown Multidisciplinary Chemistry Visceral pain General Chemistry Anatomy HEK293 Cells 030104 developmental biology Gene Expression Regulation nervous system NIH 3T3 Cells Chloride channel Calcium Female medicine.symptom Neuroscience 030217 neurology & neurosurgery |
Zdroj: | NATURE COMMUNICATIONS(7) Nature Communications Nature Communications, Vol 7, Iss 1, Pp 1-13 (2016) |
Popis: | 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. Spike-frequency adaptation in thalamocortical (TC) neurons is important for sensory transmission though the underlying mechanisms are not fully understood. Here, the authors identify a role for the calcium-activated chloride channel, ANO2, in mediating TC spiking adaptations and visceral pain response. |
Databáze: | OpenAIRE |
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