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Neurofibromatosis type 1 (NF1) is an autosomal dominant disease caused by loss-of-function mutations in  NF1  gene, which encodes a GTPase activating protein for RAS. NF1 affects multiple systems including brain and is highly associated with cognitive deficits such as learning difficulties and attention deficits. Previous studies have suggested that GABAergic inhibitory neuron is the cell type primarily responsible for the learning deficits in mouse models of NF1. However, it is not clear how NF1 mutations selectively affect inhibitory neurons in the central nervous system. In this study, we show that the expression level of  Nf1  is significantly higher in inhibitory neurons than in excitatory neurons in mouse hippocampus and cortex by using in situ hybridization. Furthermore, we also found that  NF1  is enriched in inhibitory neurons in the human cortex, confirming that the differential expressions of  NF1  between two cell types are evolutionarily conserved. Our results suggest that the enriched expression of  NF1  in inhibitory neurons may underlie inhibitory neuron-specific deficits in NF1.   Electronic supplementary material  The online version of this article (10.1186/s13041-019-0481-0) contains supplementary material, which is available to authorized users.

Enriched expression of NF1 in inhibitory neurons in both mouse and human brain