Distribution of calcitonin gene-related peptide in vertebrate neuromuscular junctions

Relationship to the acetylcholine receptor

B. Csillik, L. Tajti, T. Kovács, E. Kukla, P. Rakic, E. Knyihár-Csillik

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

Calcitonin gene-related peptide (CGRP), regarded by several authors to be involved in maintenance of the acetylcholine receptor, is present in the motor axons of various striated rat muscles. It is present, however, only in motor endplates of several selected striated muscles, where it is located in presynaptic axon terminals of neuromuscular junctions. No immunoreactivity could be seen within synaptic vesicles themselves. In the non-human primate Macaca fasciculata, neuromuscular junctions, including those in the diaphragm, display an intense CGRP reaction. The structure of the simian motor endplates is more elaborate than that of the rat. Amphibian motor nerve endings, both in tetanic and tonic muscles, display CGRP immunoreactivity. In tetanic muscles the CGRP reaction outlines 'terminaisons en placque' (true motor end plates) and weakly reacting 'terminaisons en grappe' (grape-like endings) in tonic muscles. On supramaximal stimulation of the motor nerve, CGRP is depleted from the affected neuromuscular junctions. Wallerian degeneration of the motor axon results in complete disappearance of CGRP. In most rat muscles in which motor endplates do not normally exhibit CGRP immunoreactivity, e.g., the diaphragm and buccinator muscles, the pre- terminal motor axons are CGRP-positive. After immobilization of such muscles by local bupivacaine injection to rats under brief chloral hydrate anesthesia, CGRP immunoreactivity of the neuromuscular junctions can be elicited because blockade of neuromuscular transmission results in accumulation of CGRP in the endplates. Even more striking is the appearance of CGRP immunoreactivity in normally non-reactive motor endplates during axon regeneration after an experimentally induced Wallerian degeneration of the motor axons. We conclude that CGRP is a regular, genotypically determined component of neuromuscular junctions, present either in a manifest or in a latent form. The latter can be elicited by various experimental approaches. The presence of CGRP in the motor endplate supports the theory that this peptide is instrumental in maintenance of the acetylcholine receptor.

Original languageEnglish
Pages (from-to)1547-1555
Number of pages9
JournalJournal of Histochemistry and Cytochemistry
Volume41
Issue number10
Publication statusPublished - 1993

Fingerprint

Calcitonin Gene-Related Peptide
Neuromuscular Junction
Cholinergic Receptors
Vertebrates
Motor Endplate
Muscles
Axons
Presynaptic Terminals
Wallerian Degeneration
Striated Muscle
Diaphragm
Maintenance
Chloral Hydrate
Neuromuscular Blockade
Nerve Endings
Synaptic Vesicles
Bupivacaine
Vitis
Macaca
Amphibians

Keywords

  • Acetylcholine receptor
  • Bupivacaine inactivation
  • CGRP
  • Degeneration
  • Immobilization
  • Motor endplate (mammalian, primate, amphibian)
  • Regeneration

ASJC Scopus subject areas

  • Cell Biology
  • Anatomy

Cite this

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title = "Distribution of calcitonin gene-related peptide in vertebrate neuromuscular junctions: Relationship to the acetylcholine receptor",
abstract = "Calcitonin gene-related peptide (CGRP), regarded by several authors to be involved in maintenance of the acetylcholine receptor, is present in the motor axons of various striated rat muscles. It is present, however, only in motor endplates of several selected striated muscles, where it is located in presynaptic axon terminals of neuromuscular junctions. No immunoreactivity could be seen within synaptic vesicles themselves. In the non-human primate Macaca fasciculata, neuromuscular junctions, including those in the diaphragm, display an intense CGRP reaction. The structure of the simian motor endplates is more elaborate than that of the rat. Amphibian motor nerve endings, both in tetanic and tonic muscles, display CGRP immunoreactivity. In tetanic muscles the CGRP reaction outlines 'terminaisons en placque' (true motor end plates) and weakly reacting 'terminaisons en grappe' (grape-like endings) in tonic muscles. On supramaximal stimulation of the motor nerve, CGRP is depleted from the affected neuromuscular junctions. Wallerian degeneration of the motor axon results in complete disappearance of CGRP. In most rat muscles in which motor endplates do not normally exhibit CGRP immunoreactivity, e.g., the diaphragm and buccinator muscles, the pre- terminal motor axons are CGRP-positive. After immobilization of such muscles by local bupivacaine injection to rats under brief chloral hydrate anesthesia, CGRP immunoreactivity of the neuromuscular junctions can be elicited because blockade of neuromuscular transmission results in accumulation of CGRP in the endplates. Even more striking is the appearance of CGRP immunoreactivity in normally non-reactive motor endplates during axon regeneration after an experimentally induced Wallerian degeneration of the motor axons. We conclude that CGRP is a regular, genotypically determined component of neuromuscular junctions, present either in a manifest or in a latent form. The latter can be elicited by various experimental approaches. The presence of CGRP in the motor endplate supports the theory that this peptide is instrumental in maintenance of the acetylcholine receptor.",
keywords = "Acetylcholine receptor, Bupivacaine inactivation, CGRP, Degeneration, Immobilization, Motor endplate (mammalian, primate, amphibian), Regeneration",
author = "B. Csillik and L. Tajti and T. Kov{\'a}cs and E. Kukla and P. Rakic and E. Knyih{\'a}r-Csillik",
year = "1993",
language = "English",
volume = "41",
pages = "1547--1555",
journal = "Journal of Histochemistry and Cytochemistry",
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TY - JOUR

T1 - Distribution of calcitonin gene-related peptide in vertebrate neuromuscular junctions

T2 - Relationship to the acetylcholine receptor

AU - Csillik, B.

AU - Tajti, L.

AU - Kovács, T.

AU - Kukla, E.

AU - Rakic, P.

AU - Knyihár-Csillik, E.

PY - 1993

Y1 - 1993

N2 - Calcitonin gene-related peptide (CGRP), regarded by several authors to be involved in maintenance of the acetylcholine receptor, is present in the motor axons of various striated rat muscles. It is present, however, only in motor endplates of several selected striated muscles, where it is located in presynaptic axon terminals of neuromuscular junctions. No immunoreactivity could be seen within synaptic vesicles themselves. In the non-human primate Macaca fasciculata, neuromuscular junctions, including those in the diaphragm, display an intense CGRP reaction. The structure of the simian motor endplates is more elaborate than that of the rat. Amphibian motor nerve endings, both in tetanic and tonic muscles, display CGRP immunoreactivity. In tetanic muscles the CGRP reaction outlines 'terminaisons en placque' (true motor end plates) and weakly reacting 'terminaisons en grappe' (grape-like endings) in tonic muscles. On supramaximal stimulation of the motor nerve, CGRP is depleted from the affected neuromuscular junctions. Wallerian degeneration of the motor axon results in complete disappearance of CGRP. In most rat muscles in which motor endplates do not normally exhibit CGRP immunoreactivity, e.g., the diaphragm and buccinator muscles, the pre- terminal motor axons are CGRP-positive. After immobilization of such muscles by local bupivacaine injection to rats under brief chloral hydrate anesthesia, CGRP immunoreactivity of the neuromuscular junctions can be elicited because blockade of neuromuscular transmission results in accumulation of CGRP in the endplates. Even more striking is the appearance of CGRP immunoreactivity in normally non-reactive motor endplates during axon regeneration after an experimentally induced Wallerian degeneration of the motor axons. We conclude that CGRP is a regular, genotypically determined component of neuromuscular junctions, present either in a manifest or in a latent form. The latter can be elicited by various experimental approaches. The presence of CGRP in the motor endplate supports the theory that this peptide is instrumental in maintenance of the acetylcholine receptor.

AB - Calcitonin gene-related peptide (CGRP), regarded by several authors to be involved in maintenance of the acetylcholine receptor, is present in the motor axons of various striated rat muscles. It is present, however, only in motor endplates of several selected striated muscles, where it is located in presynaptic axon terminals of neuromuscular junctions. No immunoreactivity could be seen within synaptic vesicles themselves. In the non-human primate Macaca fasciculata, neuromuscular junctions, including those in the diaphragm, display an intense CGRP reaction. The structure of the simian motor endplates is more elaborate than that of the rat. Amphibian motor nerve endings, both in tetanic and tonic muscles, display CGRP immunoreactivity. In tetanic muscles the CGRP reaction outlines 'terminaisons en placque' (true motor end plates) and weakly reacting 'terminaisons en grappe' (grape-like endings) in tonic muscles. On supramaximal stimulation of the motor nerve, CGRP is depleted from the affected neuromuscular junctions. Wallerian degeneration of the motor axon results in complete disappearance of CGRP. In most rat muscles in which motor endplates do not normally exhibit CGRP immunoreactivity, e.g., the diaphragm and buccinator muscles, the pre- terminal motor axons are CGRP-positive. After immobilization of such muscles by local bupivacaine injection to rats under brief chloral hydrate anesthesia, CGRP immunoreactivity of the neuromuscular junctions can be elicited because blockade of neuromuscular transmission results in accumulation of CGRP in the endplates. Even more striking is the appearance of CGRP immunoreactivity in normally non-reactive motor endplates during axon regeneration after an experimentally induced Wallerian degeneration of the motor axons. We conclude that CGRP is a regular, genotypically determined component of neuromuscular junctions, present either in a manifest or in a latent form. The latter can be elicited by various experimental approaches. The presence of CGRP in the motor endplate supports the theory that this peptide is instrumental in maintenance of the acetylcholine receptor.

KW - Acetylcholine receptor

KW - Bupivacaine inactivation

KW - CGRP

KW - Degeneration

KW - Immobilization

KW - Motor endplate (mammalian, primate, amphibian)

KW - Regeneration

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VL - 41

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