Synapse-specific control of synaptic efficacy at the terminals of a single neuron View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-03

AUTHORS

Graeme W. Davis, Corey S. Goodman

ABSTRACT

The regulation of synaptic efficacy is essential for the proper functioning of neural circuits. If synaptic gain is set too high or too low, cells are either activated inappropriately or remain silent. There is extra complexity because synapses are not static, but form, retract, expand, strengthen, and weaken throughout life. Homeostatic regulatory mechanisms that control synaptic efficacy presumably exist to ensure that neurons remain functional within a meaningful physiological range1,2,3,4,5. One of the best defined systems for analysis of the mechanisms that regulate synaptic efficacy is the neuromuscular junction. It has been shown, in organisms ranging from insects to humans, that changes in synaptic efficacy are tightly coupled to changes in muscle size during development1,6,7,8. It has been proposed that a signal from muscle to motor neuron maintains this coupling9. Here we show, by genetically manipulating muscle innervation, that there are two independent mechanisms by which muscle regulates synaptic efficacy at the terminals of single motor neurons. Increased muscle innervation results in a compensatory, target-specific decrease in presynaptic transmitter release, implying a retrograde regulation of presynaptic release. Decreased muscle innervation results in a compensatory increase in quantal size. More... »

PAGES

82-86

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/32176

DOI

http://dx.doi.org/10.1038/32176

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1012460050

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9510251


Indexing Status Check whether this publication has been indexed by Scopus and Web Of Science using the SN Indexing Status Tool
Incoming Citations Browse incoming citations for this publication using opencitations.net

JSON-LD is the canonical representation for SciGraph data.

TIP: You can open this SciGraph record using an external JSON-LD service: JSON-LD Playground Google SDTT

[
  {
    "@context": "https://springernature.github.io/scigraph/jsonld/sgcontext.json", 
    "about": [
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/11", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Medical and Health Sciences", 
        "type": "DefinedTerm"
      }, 
      {
        "id": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/1109", 
        "inDefinedTermSet": "http://purl.org/au-research/vocabulary/anzsrc-for/2008/", 
        "name": "Neurosciences", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Animals", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Cell Adhesion Molecules, Neuronal", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Drosophila", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Motor Neurons", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Muscles", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Mutagenesis", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Neuromuscular Junction", 
        "type": "DefinedTerm"
      }, 
      {
        "inDefinedTermSet": "https://www.nlm.nih.gov/mesh/", 
        "name": "Synapses", 
        "type": "DefinedTerm"
      }
    ], 
    "author": [
      {
        "affiliation": {
          "alternateName": "Neurobiology Division, Department of Molecular and Cell Biology, Howard Hughes Medical Institute, LSA room 519, University of California, 94720, Berkeley, California, USA", 
          "id": "http://www.grid.ac/institutes/grid.47840.3f", 
          "name": [
            "Neurobiology Division, Department of Molecular and Cell Biology, Howard Hughes Medical Institute, LSA room 519, University of California, 94720, Berkeley, California, USA"
          ], 
          "type": "Organization"
        }, 
        "familyName": "Davis", 
        "givenName": "Graeme W.", 
        "id": "sg:person.01013131614.62", 
        "sameAs": [
          "https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01013131614.62"
        ], 
        "type": "Person"
      }, 
      {
        "affiliation": {
          "alternateName": "Neurobiology Division, Department of Molecular and Cell Biology, Howard Hughes Medical Institute, LSA room 519, University of California, 94720, Berkeley, California, USA", 
          "id": "http://www.grid.ac/institutes/grid.47840.3f", 
          "name": [
            "Neurobiology Division, Department of Molecular and Cell Biology, Howard Hughes Medical Institute, LSA room 519, University of California, 94720, Berkeley, California, USA"
          ], 
          "type": "Organization"
        }, 
        "familyName": "Goodman", 
        "givenName": "Corey S.", 
        "id": "sg:person.01001367034.57", 
        "sameAs": [
          "https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01001367034.57"
        ], 
        "type": "Person"
      }
    ], 
    "citation": [
      {
        "id": "sg:pub.10.1007/bf00215114", 
        "sameAs": [
          "https://app.dimensions.ai/details/publication/pub.1044917675", 
          "https://doi.org/10.1007/bf00215114"
        ], 
        "type": "CreativeWork"
      }
    ], 
    "datePublished": "1998-03", 
    "datePublishedReg": "1998-03-01", 
    "description": "The regulation of synaptic efficacy is essential for the proper functioning of neural circuits. If synaptic gain is set too high or too low, cells are either activated inappropriately or remain silent. There is extra complexity because synapses are not static, but form, retract, expand, strengthen, and weaken throughout life. Homeostatic regulatory mechanisms that control synaptic efficacy presumably exist to ensure that neurons remain functional within a meaningful physiological range1,2,3,4,5. One of the best defined systems for analysis of the mechanisms that regulate synaptic efficacy is the neuromuscular junction. It has been shown, in organisms ranging from insects to humans, that changes in synaptic efficacy are tightly coupled to changes in muscle size during development1,6,7,8. It has been proposed that a signal from muscle to motor neuron maintains this coupling9. Here we show, by genetically manipulating muscle innervation, that there are two independent mechanisms by which muscle regulates synaptic efficacy at the terminals of single motor neurons. Increased muscle innervation results in a compensatory, target-specific decrease in presynaptic transmitter release, implying a retrograde regulation of presynaptic release. Decreased muscle innervation results in a compensatory increase in quantal size.", 
    "genre": "article", 
    "id": "sg:pub.10.1038/32176", 
    "isAccessibleForFree": false, 
    "isPartOf": [
      {
        "id": "sg:journal.1018957", 
        "issn": [
          "0028-0836", 
          "1476-4687"
        ], 
        "name": "Nature", 
        "publisher": "Springer Nature", 
        "type": "Periodical"
      }, 
      {
        "issueNumber": "6671", 
        "type": "PublicationIssue"
      }, 
      {
        "type": "PublicationVolume", 
        "volumeNumber": "392"
      }
    ], 
    "keywords": [
      "synaptic efficacy", 
      "muscle innervation", 
      "motor neurons", 
      "single motor neuron", 
      "presynaptic transmitter release", 
      "synapse-specific control", 
      "retrograde regulation", 
      "homeostatic regulatory mechanisms", 
      "presynaptic release", 
      "regulatory mechanisms", 
      "transmitter release", 
      "muscle size", 
      "compensatory increase", 
      "neuromuscular junction", 
      "neural circuits", 
      "innervation", 
      "quantal size", 
      "synaptic gain", 
      "neurons", 
      "single neurons", 
      "efficacy", 
      "independent mechanisms", 
      "muscle", 
      "regulation", 
      "proper functioning", 
      "insects", 
      "organisms", 
      "mechanism", 
      "release", 
      "synapses", 
      "cells", 
      "terminals", 
      "humans", 
      "changes", 
      "decrease", 
      "functioning", 
      "control", 
      "life", 
      "increase", 
      "junction", 
      "size", 
      "signals", 
      "gain", 
      "analysis", 
      "form", 
      "complexity", 
      "system", 
      "retract", 
      "circuit", 
      "extra complexity"
    ], 
    "name": "Synapse-specific control of synaptic efficacy at the terminals of a single neuron", 
    "pagination": "82-86", 
    "productId": [
      {
        "name": "dimensions_id", 
        "type": "PropertyValue", 
        "value": [
          "pub.1012460050"
        ]
      }, 
      {
        "name": "doi", 
        "type": "PropertyValue", 
        "value": [
          "10.1038/32176"
        ]
      }, 
      {
        "name": "pubmed_id", 
        "type": "PropertyValue", 
        "value": [
          "9510251"
        ]
      }
    ], 
    "sameAs": [
      "https://doi.org/10.1038/32176", 
      "https://app.dimensions.ai/details/publication/pub.1012460050"
    ], 
    "sdDataset": "articles", 
    "sdDatePublished": "2022-09-02T15:48", 
    "sdLicense": "https://scigraph.springernature.com/explorer/license/", 
    "sdPublisher": {
      "name": "Springer Nature - SN SciGraph project", 
      "type": "Organization"
    }, 
    "sdSource": "s3://com-springernature-scigraph/baseset/20220902/entities/gbq_results/article/article_271.jsonl", 
    "type": "ScholarlyArticle", 
    "url": "https://doi.org/10.1038/32176"
  }
]
 

Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

JSON-LD is a popular format for linked data which is fully compatible with JSON.

curl -H 'Accept: application/ld+json' 'https://scigraph.springernature.com/pub.10.1038/32176'

N-Triples is a line-based linked data format ideal for batch operations.

curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/pub.10.1038/32176'

Turtle is a human-readable linked data format.

curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/pub.10.1038/32176'

RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1038/32176'


 

This table displays all metadata directly associated to this object as RDF triples.

154 TRIPLES      21 PREDICATES      85 URIs      76 LITERALS      15 BLANK NODES

Subject Predicate Object
1 sg:pub.10.1038/32176 schema:about N042ddeba19074a0e9f556cc1a44ce8fc
2 N155c8ca0b1274896a1791b3ceb9255f9
3 N55d1b74149b6423faabff021c6db588a
4 N5d5a064d4d32448c968b839dec7a0624
5 N617d4241a7d44725966ad5e4df81ecb7
6 N92957100215c4097a718f20238929f82
7 N941115923b34465bb9ae164d6908c363
8 N947edc88cab941e6847e500a1ef825d7
9 anzsrc-for:11
10 anzsrc-for:1109
11 schema:author N6b48f34156bb4505933c37f2a109e136
12 schema:citation sg:pub.10.1007/bf00215114
13 schema:datePublished 1998-03
14 schema:datePublishedReg 1998-03-01
15 schema:description The regulation of synaptic efficacy is essential for the proper functioning of neural circuits. If synaptic gain is set too high or too low, cells are either activated inappropriately or remain silent. There is extra complexity because synapses are not static, but form, retract, expand, strengthen, and weaken throughout life. Homeostatic regulatory mechanisms that control synaptic efficacy presumably exist to ensure that neurons remain functional within a meaningful physiological range1,2,3,4,5. One of the best defined systems for analysis of the mechanisms that regulate synaptic efficacy is the neuromuscular junction. It has been shown, in organisms ranging from insects to humans, that changes in synaptic efficacy are tightly coupled to changes in muscle size during development1,6,7,8. It has been proposed that a signal from muscle to motor neuron maintains this coupling9. Here we show, by genetically manipulating muscle innervation, that there are two independent mechanisms by which muscle regulates synaptic efficacy at the terminals of single motor neurons. Increased muscle innervation results in a compensatory, target-specific decrease in presynaptic transmitter release, implying a retrograde regulation of presynaptic release. Decreased muscle innervation results in a compensatory increase in quantal size.
16 schema:genre article
17 schema:isAccessibleForFree false
18 schema:isPartOf N28f366e3b2da4363aed268e1599b887d
19 N9cb5dd2c076e44e0a614b89385d58ca7
20 sg:journal.1018957
21 schema:keywords analysis
22 cells
23 changes
24 circuit
25 compensatory increase
26 complexity
27 control
28 decrease
29 efficacy
30 extra complexity
31 form
32 functioning
33 gain
34 homeostatic regulatory mechanisms
35 humans
36 increase
37 independent mechanisms
38 innervation
39 insects
40 junction
41 life
42 mechanism
43 motor neurons
44 muscle
45 muscle innervation
46 muscle size
47 neural circuits
48 neuromuscular junction
49 neurons
50 organisms
51 presynaptic release
52 presynaptic transmitter release
53 proper functioning
54 quantal size
55 regulation
56 regulatory mechanisms
57 release
58 retract
59 retrograde regulation
60 signals
61 single motor neuron
62 single neurons
63 size
64 synapse-specific control
65 synapses
66 synaptic efficacy
67 synaptic gain
68 system
69 terminals
70 transmitter release
71 schema:name Synapse-specific control of synaptic efficacy at the terminals of a single neuron
72 schema:pagination 82-86
73 schema:productId N5739a02b35704b0ea7bf529095ddaa5a
74 Nd874a5e3a24c414d806a4ca6185f7091
75 Nf6a1316f759a4c4d9341e9549c70cdd9
76 schema:sameAs https://app.dimensions.ai/details/publication/pub.1012460050
77 https://doi.org/10.1038/32176
78 schema:sdDatePublished 2022-09-02T15:48
79 schema:sdLicense https://scigraph.springernature.com/explorer/license/
80 schema:sdPublisher N1388fda628a14671b1cc0f8210a22a28
81 schema:url https://doi.org/10.1038/32176
82 sgo:license sg:explorer/license/
83 sgo:sdDataset articles
84 rdf:type schema:ScholarlyArticle
85 N042ddeba19074a0e9f556cc1a44ce8fc schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
86 schema:name Animals
87 rdf:type schema:DefinedTerm
88 N1388fda628a14671b1cc0f8210a22a28 schema:name Springer Nature - SN SciGraph project
89 rdf:type schema:Organization
90 N155c8ca0b1274896a1791b3ceb9255f9 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
91 schema:name Mutagenesis
92 rdf:type schema:DefinedTerm
93 N28f366e3b2da4363aed268e1599b887d schema:issueNumber 6671
94 rdf:type schema:PublicationIssue
95 N55d1b74149b6423faabff021c6db588a schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
96 schema:name Neuromuscular Junction
97 rdf:type schema:DefinedTerm
98 N5739a02b35704b0ea7bf529095ddaa5a schema:name dimensions_id
99 schema:value pub.1012460050
100 rdf:type schema:PropertyValue
101 N5d5a064d4d32448c968b839dec7a0624 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
102 schema:name Cell Adhesion Molecules, Neuronal
103 rdf:type schema:DefinedTerm
104 N617d4241a7d44725966ad5e4df81ecb7 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
105 schema:name Drosophila
106 rdf:type schema:DefinedTerm
107 N6b48f34156bb4505933c37f2a109e136 rdf:first sg:person.01013131614.62
108 rdf:rest Nf45d556ef3dc44dfae5e37c34bb24e80
109 N92957100215c4097a718f20238929f82 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
110 schema:name Synapses
111 rdf:type schema:DefinedTerm
112 N941115923b34465bb9ae164d6908c363 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
113 schema:name Muscles
114 rdf:type schema:DefinedTerm
115 N947edc88cab941e6847e500a1ef825d7 schema:inDefinedTermSet https://www.nlm.nih.gov/mesh/
116 schema:name Motor Neurons
117 rdf:type schema:DefinedTerm
118 N9cb5dd2c076e44e0a614b89385d58ca7 schema:volumeNumber 392
119 rdf:type schema:PublicationVolume
120 Nd874a5e3a24c414d806a4ca6185f7091 schema:name pubmed_id
121 schema:value 9510251
122 rdf:type schema:PropertyValue
123 Nf45d556ef3dc44dfae5e37c34bb24e80 rdf:first sg:person.01001367034.57
124 rdf:rest rdf:nil
125 Nf6a1316f759a4c4d9341e9549c70cdd9 schema:name doi
126 schema:value 10.1038/32176
127 rdf:type schema:PropertyValue
128 anzsrc-for:11 schema:inDefinedTermSet anzsrc-for:
129 schema:name Medical and Health Sciences
130 rdf:type schema:DefinedTerm
131 anzsrc-for:1109 schema:inDefinedTermSet anzsrc-for:
132 schema:name Neurosciences
133 rdf:type schema:DefinedTerm
134 sg:journal.1018957 schema:issn 0028-0836
135 1476-4687
136 schema:name Nature
137 schema:publisher Springer Nature
138 rdf:type schema:Periodical
139 sg:person.01001367034.57 schema:affiliation grid-institutes:grid.47840.3f
140 schema:familyName Goodman
141 schema:givenName Corey S.
142 schema:sameAs https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01001367034.57
143 rdf:type schema:Person
144 sg:person.01013131614.62 schema:affiliation grid-institutes:grid.47840.3f
145 schema:familyName Davis
146 schema:givenName Graeme W.
147 schema:sameAs https://app.dimensions.ai/discover/publication?and_facet_researcher=ur.01013131614.62
148 rdf:type schema:Person
149 sg:pub.10.1007/bf00215114 schema:sameAs https://app.dimensions.ai/details/publication/pub.1044917675
150 https://doi.org/10.1007/bf00215114
151 rdf:type schema:CreativeWork
152 grid-institutes:grid.47840.3f schema:alternateName Neurobiology Division, Department of Molecular and Cell Biology, Howard Hughes Medical Institute, LSA room 519, University of California, 94720, Berkeley, California, USA
153 schema:name Neurobiology Division, Department of Molecular and Cell Biology, Howard Hughes Medical Institute, LSA room 519, University of California, 94720, Berkeley, California, USA
154 rdf:type schema:Organization
 




Preview window. Press ESC to close (or click here)


...