Primary Cilia Signaling Shapes the Development of Interneuronal Connectivity
Open accessAbstract
Appropriate growth and synaptic integration of GABAergic inhibitory interneurons are essential for functional neural circuits in the brain. Here, we demonstrate that disruption of primary cilia function following the selective loss of ciliary GTPase Arl13b in interneurons impairs interneuronal morphology and synaptic connectivity, leading to altered excitatory/inhibitory activity balance. The altered morphology and connectivity of cilia mutant interneurons and the functional deficits are rescued by either chemogenetic activation of ciliary G-protein-coupled receptor (GPCR) signaling or the selective induction of Sstr3, a ciliary GPCR, in Arl13b-deficient cilia. Our results thus define a specific requirement for primary cilia-mediated GPCR signaling in interneuronal connectivity and inhibitory circuit formation.
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Ciliary export of activated SSTR3 in cultured renal epithelial cells requires beta-arrestin-2.
“ciliary export of activated SSTR3 in cultured renal epithelial cells also requires β-arrestin-2 28, 172.”
From Cellular signalling by primary cilia in development, organ function and disease (2019) · cites this paper as [172]
The Discussion (page not provided) reports that activated GPCRs such as Sstr3 can leave ciliary tips by ectocytosis. It does not say that this export requires β-arrestin-2 or that the finding concerns cultured renal epithelial cells; the Results instead examine Sstr3 in interneurons. (LLM, conf=0.85)
Experimental — accuracy not yet measuredCiliary dysfunction associated with Aβ has been reported to reduce the connectivity of neuronal circuits and cause synapse loss.
“Ciliary dysfunction associated with Aβ has been reported to reduce the connectivity of neuronal circuits and cause synapse loss [25, 75].”
From Abnormal accumulation of extracellular vesicles in hippocampal dystrophic axons and regulation by the primary cilia in Alzheimer's disease (2023) · cites this paper as [25]
The Results section, “Primary ciliary signaling is required for IN synaptic connection” (page unavailable), reports reduced synaptic bouton density and size after ciliary Arl13b deletion, supporting impaired interneuronal connectivity and fewer synaptic boutons. The paper does not associate this dysfunction with Aβ, so it does not support that qualifier. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPrimary cilia length plays a critical role in the proper formation and function of synapses, which is an important pathological feature of AD.
“Collectively, these findings underscore the critical role of primary cilia length in the proper formation and function of synapses, which is an important pathological feature of AD.”
From Changes of the Primary Cilia in Alzheimer's Disease Pathogenesis (2025) · cites this paper as Guo et al. 2017
The Introduction and Results (page numbers unavailable) show that disrupting primary cilia signaling impairs interneuronal connectivity and inhibitory synaptic activity. They do not establish that cilia length is critical to synapse formation or function, or link this finding to Alzheimer’s disease (AD). (LLM, conf=0.88)
Experimental — accuracy not yet measuredSuch defects can be rescued by activating ciliary G-protein-coupled receptors (GPCRs), highlighting the significance of these receptors on primary cilia for neural circuit formation.
“Such defects can be rescued by activating ciliary G-protein-coupled receptors (GPCRs), highlighting the significance of these receptors on primary cilia for neural circuit formation.”
From Changes of the Primary Cilia in Alzheimer's Disease Pathogenesis (2025) · cites this paper as Guo et al. 2017
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References 89 · Cited by 136
- Authors
- Guo, J., Otis, J. M., Higginbotham, H., Monckton, C., Cheng, J., Asokan, A., Mykytyn, K., Caspary, T., Stuber, G. D., & Anton, E. S.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- The Ohio State University (US)
- Emory University (US)
- Corresponding author
- Anton, E.S.
- ORCID
- Venue
- Developmental Cell
- Publisher
- Elsevier BV
- Published
- 2017-08
- Volume
- 42
- Issue
- 3
- Pages
- 286-300.e4
- ISSN
- 1534-5807 (ISSN-L)
- PMC
- PMC5571900
- OpenAlex
- W2742431958
- Cited by
- 136
- References
- 89
- Citations by year
- 2026: 14 · 2025: 20 · 2024: 21 · 2023: 16 · 2022: 13 · 2021: 19 · 2020: 14 · 2019: 14 · 2018: 3 · 2017: 2
- FWCI
- 5.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Developmental Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (NS 090029, MH060929)
- NINDS (5P30NS045892)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Kidney Cyst Diseases
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- primary cilia, ARL13B, GABAergic interneurons, synaptic integration, excitation-inhibition balance, SSTR3, ciliary signaling, interneuron morphology, inhibitory circuits
- MeSH terms
- Animals, Cells, Cultured, Cilia, Interneurons, Synapses, Signal Transduction, Receptors, Somatostatin, ADP-Ribosylation Factors, Mice, Synaptic Potentials, Neurogenesis
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