Primary cilia in the postnatal brain: Subcellular compartments for organizing neuromodulatory signaling
Primary cilia have well characterized roles in early brain development, relaying signals critical for neurogenesis and brain formation during embryonic stages. Less understood are the contributions of cilia-mediated signaling to postnatal brain function. Several cilia-localized receptors that bind n...
Saved in:
Published in | Current opinion in neurobiology Vol. 74; p. 102533 |
---|---|
Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier Ltd
01.06.2022
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Primary cilia have well characterized roles in early brain development, relaying signals critical for neurogenesis and brain formation during embryonic stages. Less understood are the contributions of cilia-mediated signaling to postnatal brain function. Several cilia-localized receptors that bind neuropeptides and neurotransmitters endogenous to the brain have been identified in adult neurons, but the functional significance of signaling through these cilia-localized receptors is largely unexplored. Ciliopathic disorders in humans often manifest with neurodevelopmental abnormalities and cognitive deficits. Intriguingly, recent research has also linked several neuropsychiatric disorders and neurodegenerative diseases to ciliary dysfunction. This review summarizes recent evidence suggesting that cilia signaling may dynamically regulate postnatal neuronal physiology and connectivity, and highlights possible links among cilia, neuronal circuitry, neuron survival, and neurological disorders.
•Primary cilia are maintained on most neurons and astrocytes in the postnatal brain.•Ciliary transduction of neuromodulatory signals regulates synaptic properties.•Ciliary signaling acts on acute and chronic timescales to regulate circuit function.•Cilia dysfunction is linked to neuropsychiatric and neurodegenerative disorders. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 0959-4388 1873-6882 1873-6882 |
DOI: | 10.1016/j.conb.2022.102533 |