期刊
NEURON
卷 53, 期 1, 页码 39-52出版社
CELL PRESS
DOI: 10.1016/j.neuron.2006.11.015
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资金
- MRC [MC_U105185857] Funding Source: UKRI
- Medical Research Council [MC_U105185857] Funding Source: researchfish
- Medical Research Council [MC_U105185857] Funding Source: Medline
- NIDA NIH HHS [R01 DA016445, R01DA016445-01] Funding Source: Medline
- NIGMS NIH HHS [R01 GM057918, GM057918] Funding Source: Medline
- NIMH NIH HHS [T32 MH018882] Funding Source: Medline
- NINDS NIH HHS [R01 NS036918, NS036918] Funding Source: Medline
Signal transduction through heterotrimeric G proteins is critical for sensory response across species. Regulator of G protein signaling (RGS) proteins are negative regulators of signal transduction. Herein we describe a role for C. elegans RGS-3 in the regulation of sensory behaviors. rgs-3 mutant animals fail to respond to intense sensory stimuli but respond normally to low concentrations of specific odorants. We find that loss of RGS-3 leads to aberrantly increased G protein-coupled calcium signaling but decreased synaptic output, ultimately leading to behavioral defects. Thus, rgs-3 responses are restored by decreasing G protein-coupled signal transduction, either genetically or by exogenous dopamine, by expressing a calcium-binding protein to buffer calcium levels in sensory neurons or by enhancing glutamatergic synaptic transmission from sensory neurons. Therefore, while RGS proteins generally act to downregulate signaling, loss of a specific RGS protein in sensory neurons can lead to defective responses to external stimuli.
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