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电压门控钙通道作用于腺苷酸环化酶 Ac78C 的上游，以促进树突再生的及时启动。

Voltage-gated calcium channels act upstream of adenylyl cyclase Ac78C to promote timely initiation of dendrite regeneration.

机构信息

Biochemistry and Molecular Biology and the Huck Institutes of the Life Sciences The Pennsylvania State University, University Park, Pennsylvania, United States of America.

出版信息

PLoS Genet. 2024 Aug 26;20(8):e1011388. doi: 10.1371/journal.pgen.1011388. eCollection 2024 Aug.

DOI:10.1371/journal.pgen.1011388
PMID:39186815
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11379402/
Abstract

Most neurons are not replaced after injury and thus possess robust intrinsic mechanisms for repair after damage. Axon injury triggers a calcium wave, and calcium and cAMP can augment axon regeneration. In comparison to axon regeneration, dendrite regeneration is poorly understood. To test whether calcium and cAMP might also be involved in dendrite injury signaling, we tracked the responses of Drosophila dendritic arborization neurons to laser severing of axons and dendrites. We found that calcium and subsequently cAMP accumulate in the cell body after both dendrite and axon injury. Two voltage-gated calcium channels (VGCCs), L-Type and T-Type, are required for the calcium influx in response to dendrite injury and play a role in rapid initiation of dendrite regeneration. The AC8 family adenylyl cyclase, Ac78C, is required for cAMP production after dendrite injury and timely initiation of regeneration. Injury-induced cAMP production is sensitive to VGCC reduction, placing calcium upstream of cAMP generation. We propose that two VGCCs initiate global calcium influx in response to dendrite injury followed by production of cAMP by Ac78C. This signaling pathway promotes timely initiation of dendrite regrowth several hours after dendrite damage.

摘要

大多数神经元在受伤后不会被替换，因此它们具有强大的内在修复机制。轴突损伤会引发钙波，钙和 cAMP 可以增强轴突再生。与轴突再生相比，树突再生的研究还很不充分。为了测试钙和 cAMP 是否也参与树突损伤信号转导，我们跟踪了果蝇树突分枝神经元对轴突和树突激光切断的反应。我们发现，钙随后在细胞体中积累，无论是在轴突还是树突损伤后。两种电压门控钙通道（VGCCs），L 型和 T 型，对于响应树突损伤的钙内流是必需的，并在树突再生的快速启动中发挥作用。AC8 家族腺苷酸环化酶 Ac78C 在树突损伤后产生 cAMP，对于树突再生的及时启动是必需的。损伤诱导的 cAMP 产生对 VGCC 减少敏感，将钙置于 cAMP 产生的上游。我们提出，两个 VGCC 响应树突损伤引发全局钙内流，随后由 Ac78C 产生 cAMP。这种信号通路可以促进树突损伤数小时后及时启动树突再生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/2531f29f70e2/pgen.1011388.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/cb984741be24/pgen.1011388.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/874a8ed086b2/pgen.1011388.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/4c0bb641ccda/pgen.1011388.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/68afb1158834/pgen.1011388.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/385fbcbab1d9/pgen.1011388.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/673b461a2a1f/pgen.1011388.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/2531f29f70e2/pgen.1011388.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/cb984741be24/pgen.1011388.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/bf7a068d32e7/pgen.1011388.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/874a8ed086b2/pgen.1011388.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/4c0bb641ccda/pgen.1011388.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/68afb1158834/pgen.1011388.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/385fbcbab1d9/pgen.1011388.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/673b461a2a1f/pgen.1011388.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4475/11379402/2531f29f70e2/pgen.1011388.g008.jpg

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