期刊
NEURON
卷 65, 期 6, 页码 886-898出版社
CELL PRESS
DOI: 10.1016/j.neuron.2010.02.025
关键词
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资金
- Jane Coffin Childs Fellowship
- Dystonia Medical Research Foundation Fellowship
- NIH [R01-NS-028829]
- Developmental Disabilities Mental Retardation Research Center [NIH-P30-HD-18655]
Itch is the least well understood of all the somatic senses, and the neural circuits that underlie this sensation are poorly defined. Here we show that the atonal-related transcription factor Bhlhb5 is transiently expressed in the dorsal horn of the developing spinal cord and appears to play a role in the formation and regulation of pruritic (itch) circuits. Mice lacking Bhlhb5 develop self-inflicted skin lesions and show significantly enhanced scratching responses to pruritic agents. Through genetic fate-mapping and conditional ablation, we provide evidence that the pruritic phenotype in Bhlhb5 mutants is due to selective loss of a subset of inhibitory interneurons in the dorsal horn. Our findings suggest that Bhlhb5 is required for the survival of a specific population of inhibitory interneurons that regulate pruritis, and provide evidence that the loss of inhibitory synaptic input results in abnormal itch.
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