Social behavioral deficits in NF1 emerge from peripheral chemosensory neuron dysfunction

摘要: Abstract Neurofibromatosis type 1 (NF1) is a neurodevelopmental disorder commonly associated with social and communicative disabilities. The cellular circuit mechanisms by which loss of neurofibromin (Nf1) function results in deficits are unknown. Here, we identify behavioral dysregulation Nf1 Drosophila. These map to primary dysfunction small group peripheral sensory neurons, rather than central brain circuits. Specifically, regulation Ras signaling adult, Ppk23+ chemosensory cells required for normal behaviors flies. Loss attenuated ppk23+ neuronal activity response pheromonal cues, circuit-specific manipulation expression or neurons rescues deficits. Unexpectedly, this disrupted processing gives rise persistent changes behavior lasting beyond the interaction, indicating sustained effect an acute misperception. Together our data specific mechanism through acts regulate behaviors, suggest NF1 arise from propagation misinformation.