Abstract
Primary cilia are tiny microtubule-based signaling devices that regulate a variety of physiological functions, including metabolism and cell division. Defects in primary cilia lead to a myriad of diseases in humans such as obesity and cancers. In the mature brain, both neurons and astrocytes contain a single primary cilium. Although neuronal primary cilia are not directly involved in synaptic communication, their pathophysiological impacts on obesity and mental disorders are well recognized. In contrast, research on astrocytic primary cilia lags far behind. Currently, little is known about their functions and molecular pathways in the mature brain. Unlike neurons, postnatal astrocytes retain the capacity of cell division and can become reactive and proliferate in response to various brain insults such as epilepsy, ischemia, traumatic brain injury, and neurodegenerative β-amyloid plaques. Since primary cilia derive from the mother centrioles, astrocyte proliferation must occur in coordination with the dismantling and ciliogenesis of astrocyte cilia. In this regard, the functions, signal pathways, and structural dynamics of neuronal and astrocytic primary cilia are fundamentally different. Here we discuss and compare the current understanding of neuronal and astrocytic primary cilia.