Ionizing radiation can cause changes in nervous system function. However, the underlying mechanism remains unclear. In this study, Caenorhabditis elegans (C. elegans) was irradiated with 75 Gy of <sup>60</sup>Co whole-body &#
x3b3; radiation. Behavioral indicators (head thrashes, touch avoidance, and foraging), and the development of dopaminergic neurons related to behavioral function, were evaluated to assess the effects of ionizing radiation on nervous system function in C. elegans. Various behaviors were impaired after whole-body irradiation and degeneration of dopamine neurons was observed. This suggests that 75 Gy of &#
x3b3; radiation is sufficient to induce nervous system dysfunction. The genes
nhr-76 and
crm-1, which are reported to be related to nervous system function in human and mouse, were screened by transcriptome sequencing and bioinformatics analysis after irradiation or sham irradiation. The expression levels of these two genes were increased after radiation. Next, RNAi technology was used to inhibit the expression of
crm-1, a gene whose homologs are associated with motor neuron development in other species. Downregulation of
crm-1 expression effectively alleviated the deleterious effects of ionizing radiation on head thrashes and touch avoidance. It was also found that the expression level of
crm-1 was regulated by the nuclear receptor gene
nhr-76. The results of this study suggest that knocking down the expression level of
nhr-76 can reduce the expression level of
crm-1, while down-regulating the expression level of
crm-1 can alleviate behavioral disorders induced by ionizing radiation. Therefore, inhibition of
crm-1 may be of interest as a potential therapeutic target for ionizing radiation-induced neurological dysfunction.