Neuronal and astrocytic primary cilia in the mature brain

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.

Keywords: ARL13B; Astrocytes; Primary cilia; Sonic Hedgehog; Type 3 adenylyl cyclase (AC3).

Figure 1.

Neuronal and astrocytic primary cilia are marked by AC3 and ARL13B, respectively, while microglia do not posess primary cilia. (A) AC3 is highly expressed in neuronal primary cilia, but not well expressed GFAP-labeled astrocyte cilia. (B) IBA1-marked microglia lack AC3-stained primary cilia. (C) ARL13B is highly expressed in astrocyte primary cilia. (D) IBA1-marked microglia lack ARL13B-stained primary cilia. All images were taken from the mouse hippocampus.