The Primary Cilia are Associated with the Axon Initial Segment in Neurons

Abstract The primary cilia serve as pivotal mediators of environmental signals and play crucial roles in neuronal responses. Disruption of ciliary function has been implicated in neuronal circuit disorders and aberrant neuronal excitability. However, the precise mechanisms remain elusive. To study t...

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Main Authors: Han Wang, Yu Li, Xin Li, Zehui Sun, Fengdan Yu, Abolghasem Pashang, Don Kulasiri, Hung Wing Li, Huan Chen, Hongwei Hou, Yan Zhang
Format: Article
Language:English
Published: Wiley 2025-03-01
Series:Advanced Science
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Online Access:https://doi.org/10.1002/advs.202407405
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author Han Wang
Yu Li
Xin Li
Zehui Sun
Fengdan Yu
Abolghasem Pashang
Don Kulasiri
Hung Wing Li
Huan Chen
Hongwei Hou
Yan Zhang
author_facet Han Wang
Yu Li
Xin Li
Zehui Sun
Fengdan Yu
Abolghasem Pashang
Don Kulasiri
Hung Wing Li
Huan Chen
Hongwei Hou
Yan Zhang
author_sort Han Wang
collection DOAJ
description Abstract The primary cilia serve as pivotal mediators of environmental signals and play crucial roles in neuronal responses. Disruption of ciliary function has been implicated in neuronal circuit disorders and aberrant neuronal excitability. However, the precise mechanisms remain elusive. To study the link between the primary cilia and neuronal excitability, manipulation of somatostatin receptor 3 (SSTR3) is investigated, as an example of how alterations in ciliary signaling may affect neuronal activity. It is found that aberrant SSTR3 expression perturbed not only ciliary morphology but also disrupted ciliary signaling cascades. Genetic deletion of SSTR3 resulted in perturbed spatial memory and synaptic plasticity. The axon initial segment (AIS) is a specialized region in the axon where action potentials are initiated. Interestingly, loss of ciliary SSTR3 led to decrease of Akt‐dependent cyclic AMP‐response element binding protein (CREB)‐mediated transcription at the AIS, specifically downregulating AIS master organizer adaptor protein ankyrin G (AnkG) expression. In addition, alterations of other ciliary proteins serotonin 6 receptor (5‐HT6R)and intraflagellar transport protein 88 (IFT88) also induced length changes of the AIS. The findings elucidate a specific interaction between the primary cilia and AIS, providing insight into the impact of the primary cilia on neuronal excitability and circuit integrity.
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spelling doaj-art-9a22a16ebd684cc6b297dd4bce51910e2025-08-20T03:24:44ZengWileyAdvanced Science2198-38442025-03-01129n/an/a10.1002/advs.202407405The Primary Cilia are Associated with the Axon Initial Segment in NeuronsHan Wang0Yu Li1Xin Li2Zehui Sun3Fengdan Yu4Abolghasem Pashang5Don Kulasiri6Hung Wing Li7Huan Chen8Hongwei Hou9Yan Zhang10State Key Laboratory of Membrane Biology School of Life Sciences Peking University Beijing 100871 ChinaState Key Laboratory of Membrane Biology School of Life Sciences Peking University Beijing 100871 ChinaBeijing Life Science Academy Beijing 102200 ChinaState Key Laboratory of Membrane Biology School of Life Sciences Peking University Beijing 100871 ChinaState Key Laboratory of Membrane Biology School of Life Sciences Peking University Beijing 100871 ChinaCentre for Advanced Computational Solutions (C‐fACS) AGLS faculty Lincoln University Canterbury 7647 New ZealandCentre for Advanced Computational Solutions (C‐fACS) AGLS faculty Lincoln University Canterbury 7647 New ZealandDepartment of Chemistry The Chinese University of Hong Kong Hong Kong 999077 ChinaBeijing Life Science Academy Beijing 102200 ChinaBeijing Life Science Academy Beijing 102200 ChinaState Key Laboratory of Membrane Biology School of Life Sciences Peking University Beijing 100871 ChinaAbstract The primary cilia serve as pivotal mediators of environmental signals and play crucial roles in neuronal responses. Disruption of ciliary function has been implicated in neuronal circuit disorders and aberrant neuronal excitability. However, the precise mechanisms remain elusive. To study the link between the primary cilia and neuronal excitability, manipulation of somatostatin receptor 3 (SSTR3) is investigated, as an example of how alterations in ciliary signaling may affect neuronal activity. It is found that aberrant SSTR3 expression perturbed not only ciliary morphology but also disrupted ciliary signaling cascades. Genetic deletion of SSTR3 resulted in perturbed spatial memory and synaptic plasticity. The axon initial segment (AIS) is a specialized region in the axon where action potentials are initiated. Interestingly, loss of ciliary SSTR3 led to decrease of Akt‐dependent cyclic AMP‐response element binding protein (CREB)‐mediated transcription at the AIS, specifically downregulating AIS master organizer adaptor protein ankyrin G (AnkG) expression. In addition, alterations of other ciliary proteins serotonin 6 receptor (5‐HT6R)and intraflagellar transport protein 88 (IFT88) also induced length changes of the AIS. The findings elucidate a specific interaction between the primary cilia and AIS, providing insight into the impact of the primary cilia on neuronal excitability and circuit integrity.https://doi.org/10.1002/advs.2024074055‐HT6Raxon initial segmentciliary GPCRprimary ciliaSSTR3
spellingShingle Han Wang
Yu Li
Xin Li
Zehui Sun
Fengdan Yu
Abolghasem Pashang
Don Kulasiri
Hung Wing Li
Huan Chen
Hongwei Hou
Yan Zhang
The Primary Cilia are Associated with the Axon Initial Segment in Neurons
Advanced Science
5‐HT6R
axon initial segment
ciliary GPCR
primary cilia
SSTR3
title The Primary Cilia are Associated with the Axon Initial Segment in Neurons
title_full The Primary Cilia are Associated with the Axon Initial Segment in Neurons
title_fullStr The Primary Cilia are Associated with the Axon Initial Segment in Neurons
title_full_unstemmed The Primary Cilia are Associated with the Axon Initial Segment in Neurons
title_short The Primary Cilia are Associated with the Axon Initial Segment in Neurons
title_sort primary cilia are associated with the axon initial segment in neurons
topic 5‐HT6R
axon initial segment
ciliary GPCR
primary cilia
SSTR3
url https://doi.org/10.1002/advs.202407405
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