Pickpocket1 Is an Ionotropic Molecular Sensory Transducer

被引:17
作者
Boiko, Nina [1 ]
Kucher, Volodymyr [1 ]
Stockand, James D. [1 ]
Eaton, Benjamin A. [1 ]
机构
[1] Univ Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USA
基金
美国国家卫生研究院;
关键词
SENSING ION CHANNELS; CAENORHABDITIS-ELEGANS; MECHANOSENSORY TRANSDUCTION; DROSOPHILA-MELANOGASTER; TRP CHANNELS; C-ELEGANS; DEG/ENAC; NEURONS; SUBUNIT; MEC-4;
D O I
10.1074/jbc.M112.411736
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The molecular transformation of an external stimulus into changes in sensory neuron activity is incompletely described. Although a number of molecules have been identified that can respond to stimuli, evidence that these molecules can transduce stimulation into useful neural activity is lacking. Here we demonstrate that pickpocket1 (ppk1), a Drosophila homolog of mammalian Degenerin/epithelial sodium channels, encodes an acid-sensing sodium channel that conducts a transient depolarizing current in multidendritic sensory neurons of Drosophila melanogaster. Stimulation of Ppk1 is sufficient to bring these sensory neurons to threshold, eliciting a burst of action potentials. The transient nature of the neural activity produced by Ppk1 activation is the result of Ppk1 channel gating properties. This model is supported by the observation of enhanced bursting activity in neurons expressing a gain of function ppk1 mutant harboring the degenerin mutation. These findings demonstrate that Ppk1 can function as an ionotropic molecular sensory transducer capable of transforming the perception of a stimulus into phasic neuronal activity in sensory neurons.
引用
收藏
页码:39878 / 39886
页数:9
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