Primary cilia are centriole-derived sensory organelles that are present in most mammalian cells, including astrocytes and neurons. Evidence is emerging that astrocyte and neuronal primary cilia demonstrate a dichotomy in the mature mouse brain. However, it is unknown how astrocytic and neuronal primary cilia change morphology and ciliary components when exposed to reactive insults including epilepsy and traumatic brain injury. We used a double transgenic mouse strain (Arl13b-mCherry; Centrin2-GFP), in which we found spontaneous seizures, and a cortical injury model to examine the morphological changes of astrocyte and neuronal primary cilia under reactive conditions. Transgenic overexpression of Arl13b drastically increases the length of astrocyte and neuronal primary cilia in the hippocampus, as well as cilia lengths of cultured astrocytes. Spontaneous seizures shorten Arl13b-positive astrocyte cilia and AC3-positive neuronal cilia in the hippocampus. In a cortical injury model, Arl13b-positive astrocyte cilia are not detectable, but Arl13b protein relocates to the cell body and has robust expression in the proximity of injured tissues. In contrast, the number of AC3-positive cilia near injured tissues remains unchanged, but their lengths become shorter. These results on astrocyte cilia implicate Arl13b in regulating astrocyte proliferation and tissue regeneration, while the shortening of AC3-positive cilia suggests adaptive changes of neuronal primary cilia under reactive insults.