Redistribution of Cav2.1 channels and calcium ions in nerve terminals following end-to-side neurorrhaphy

ionic imaging analysis by TOF–SIMS

Chiung Hui Liu, Hung Ming Chang, To Jung Tseng, Chyn Tair Lan, Li You Chen, Su Chung Youn, Jian Jr Lee, Fu Der Mai, Jui Feng Chou, Wen Chieh Liao

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The P/Q-type voltage-dependent calcium channel (Cav2.1) in the presynaptic membranes of motor nerve terminals plays an important role in regulating Ca2+ transport, resulting in transmitter release within the nervous system. The recovery of Ca2+-dependent signal transduction on motor end plates (MEPs) and innervated muscle may directly reflect nerve regeneration following peripheral nerve injury. Although the functional significance of calcium channels and the levels of Ca2+ signalling in nerve regeneration are well documented, little is known about calcium channel expression and its relation with the dynamic Ca2+ ion distribution at regenerating MEPs. In the present study, end-to-side neurorrhaphy (ESN) was performed as an in vivo model of peripheral nerve injury. The distribution of Ca2+ at regenerating MEPs following ESN was first detected by time-of-flight secondary ion mass spectrometry, and the specific localization and expression of Cav2.1 channels were examined by confocal microscopy and western blotting. Compared with other fundamental ions, such as Na+ and K+, dramatic changes in the Ca2+ distribution were detected along with the progression of MEP regeneration. The re-establishment of Ca2+ distribution and intensity were correlated with the functional recovery of muscle in ESN rats. Furthermore, the re-clustering of Cav2.1 channels after ESN at the nerve terminals corresponded with changes in the Ca2+ distribution. These results indicated that renewal of the Cav2.1 distribution within the presynaptic nerve terminals may be necessary for initiating a proper Ca2+ influx and shortening the latency of muscle contraction during nerve regeneration.

Original languageEnglish
Pages (from-to)1-10
Number of pages10
JournalHistochemistry and Cell Biology
DOIs
Publication statusPublished - 2016

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Motor Endplate
Calcium Channels
Nerve Regeneration
Peripheral Nerve Injuries
Secondary Ion Mass Spectrometry
Ions
Muscles
Presynaptic Terminals
Muscle Contraction
Confocal Microscopy
Nervous System
Cluster Analysis
Regeneration
Signal Transduction
Western Blotting
voltage-dependent calcium channel (P-Q type)
Membranes

Keywords

  • Ca channel
  • End-to-side neurorrhaphy
  • Nerve regeneration
  • TOF–SIMS

ASJC Scopus subject areas

  • Cell Biology
  • Histology
  • Medical Laboratory Technology
  • Molecular Biology

Cite this

Redistribution of Cav2.1 channels and calcium ions in nerve terminals following end-to-side neurorrhaphy : ionic imaging analysis by TOF–SIMS. / Liu, Chiung Hui; Chang, Hung Ming; Tseng, To Jung; Lan, Chyn Tair; Chen, Li You; Youn, Su Chung; Lee, Jian Jr; Mai, Fu Der; Chou, Jui Feng; Liao, Wen Chieh.

In: Histochemistry and Cell Biology, 2016, p. 1-10.

Research output: Contribution to journalArticle

Liu, Chiung Hui ; Chang, Hung Ming ; Tseng, To Jung ; Lan, Chyn Tair ; Chen, Li You ; Youn, Su Chung ; Lee, Jian Jr ; Mai, Fu Der ; Chou, Jui Feng ; Liao, Wen Chieh. / Redistribution of Cav2.1 channels and calcium ions in nerve terminals following end-to-side neurorrhaphy : ionic imaging analysis by TOF–SIMS. In: Histochemistry and Cell Biology. 2016 ; pp. 1-10.
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AU - Tseng, To Jung

AU - Lan, Chyn Tair

AU - Chen, Li You

AU - Youn, Su Chung

AU - Lee, Jian Jr

AU - Mai, Fu Der

AU - Chou, Jui Feng

AU - Liao, Wen Chieh

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AB - The P/Q-type voltage-dependent calcium channel (Cav2.1) in the presynaptic membranes of motor nerve terminals plays an important role in regulating Ca2+ transport, resulting in transmitter release within the nervous system. The recovery of Ca2+-dependent signal transduction on motor end plates (MEPs) and innervated muscle may directly reflect nerve regeneration following peripheral nerve injury. Although the functional significance of calcium channels and the levels of Ca2+ signalling in nerve regeneration are well documented, little is known about calcium channel expression and its relation with the dynamic Ca2+ ion distribution at regenerating MEPs. In the present study, end-to-side neurorrhaphy (ESN) was performed as an in vivo model of peripheral nerve injury. The distribution of Ca2+ at regenerating MEPs following ESN was first detected by time-of-flight secondary ion mass spectrometry, and the specific localization and expression of Cav2.1 channels were examined by confocal microscopy and western blotting. Compared with other fundamental ions, such as Na+ and K+, dramatic changes in the Ca2+ distribution were detected along with the progression of MEP regeneration. The re-establishment of Ca2+ distribution and intensity were correlated with the functional recovery of muscle in ESN rats. Furthermore, the re-clustering of Cav2.1 channels after ESN at the nerve terminals corresponded with changes in the Ca2+ distribution. These results indicated that renewal of the Cav2.1 distribution within the presynaptic nerve terminals may be necessary for initiating a proper Ca2+ influx and shortening the latency of muscle contraction during nerve regeneration.

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