Decoding the intensity of sensory input by two glutamate receptors in one C. elegans interneuron

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作者
Wenjuan Zou
Jiajun Fu
Haining Zhang
Kang Du
Wenming Huang
Junwei Yu
Shitian Li
Yuedan Fan
Howard A. Baylis
Shangbang Gao
Rui Xiao
Wei Ji
Lijun Kang
Tao Xu
机构
[1] Chinese Academy of Sciences,National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics
[2] Huazhong University of Science and Technology,Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology
[3] Zhejiang University School of Medicine,Institute of Neuroscience and Department of Neurosurgery of the First Affiliated Hospital, Department of Neurobiology, NHC and CAMS Key Laboratory of Medical Neurobiology
[4] University of Chinese Academy of Sciences,College of Life Sciences
[5] University of Cambridge,Department of Zoology
[6] University of Florida,Department of Aging and Geriatric Research, Institute of Aging, College of Medicine, Center for Smell and Taste
[7] Chinese Academy of Sciences,Center for Biological Instrument Development, Core Facility for Protein Research, Institute of Biophysics
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How neurons are capable of decoding stimulus intensity and translate this information into complex behavioral outputs is poorly defined. Here, we demonstrate that the C. elegans interneuron AIB regulates two types of behaviors: reversal initiation and feeding suppression in response to different concentrations of quinine. Low concentrations of quinine are decoded in AIB by a low-threshold, fast-inactivation glutamate receptor GLR-1 and translated into reversal initiation. In contrast, high concentrations of quinine are decoded by a high-threshold, slow-inactivation glutamate receptor GLR-5 in AIB. After activation, GLR-5 evokes sustained Ca2+ release from the inositol 1,4,5-trisphosphate (IP3)-sensitive Ca2+ stores and triggers neuropeptide secretion, which in turn activates the downstream neuron RIM and inhibits feeding. Our results reveal that distinct signal patterns in a single interneuron AIB can encode differential behavioral outputs depending on the stimulus intensity, thus highlighting the importance of functional mapping of information propagation at the single-neuron level during connectome construction.
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