Neurogenic potential of the vestibular nuclei and behavioural recovery time course in the adult cat are governed by the nature of the vestibular damage.
Identifieur interne : 000C08 ( Main/Curation ); précédent : 000C07; suivant : 000C09Neurogenic potential of the vestibular nuclei and behavioural recovery time course in the adult cat are governed by the nature of the vestibular damage.
Auteurs : Sophie Dutheil [France] ; Michel Lacour ; Brahim TighiletSource :
- PloS one [ 1932-6203 ] ; 2011.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Astrocytes (anatomopathologie), Astrocytes (métabolisme), Chats (MeSH), Comportement animal (physiologie), Différenciation cellulaire (MeSH), Facteurs temps (MeSH), Glutamate decarboxylase (métabolisme), Labyrinthe vestibulaire (anatomopathologie), Labyrinthe vestibulaire (innervation), Labyrinthe vestibulaire (physiopathologie), Neurogenèse (MeSH), Neurones afférents (anatomopathologie), Neurones afférents (métabolisme), Noyaux vestibulaires (anatomopathologie), Noyaux vestibulaires (enzymologie), Noyaux vestibulaires (physiopathologie), Prolifération cellulaire (MeSH), Protéine gliofibrillaire acide (métabolisme), Récupération fonctionnelle (physiologie), Survie cellulaire (MeSH), Vieillissement (anatomopathologie).
- MESH :
- anatomopathologie : Astrocytes, Labyrinthe vestibulaire, Neurones afférents, Noyaux vestibulaires, Vieillissement.
- enzymologie : Noyaux vestibulaires.
- métabolisme : Astrocytes, Glutamate decarboxylase, Labyrinthe vestibulaire, Neurones afférents, Protéine gliofibrillaire acide.
- physiologie : Comportement animal, Récupération fonctionnelle.
- physiopathologie : Labyrinthe vestibulaire, Noyaux vestibulaires.
- Animaux, Chats, Différenciation cellulaire, Facteurs temps, Neurogenèse, Prolifération cellulaire, Survie cellulaire.
English descriptors
- KwdEn :
- Aging (pathology), Animals (MeSH), Astrocytes (metabolism), Astrocytes (pathology), Behavior, Animal (physiology), Cats (MeSH), Cell Differentiation (MeSH), Cell Proliferation (MeSH), Cell Survival (MeSH), Glial Fibrillary Acidic Protein (metabolism), Glutamate Decarboxylase (metabolism), Neurogenesis (MeSH), Neurons, Afferent (metabolism), Neurons, Afferent (pathology), Recovery of Function (physiology), Time Factors (MeSH), Vestibular Nuclei (enzymology), Vestibular Nuclei (pathology), Vestibular Nuclei (physiopathology), Vestibule, Labyrinth (innervation), Vestibule, Labyrinth (pathology), Vestibule, Labyrinth (physiopathology).
- MESH :
- chemical , metabolism : Glial Fibrillary Acidic Protein, Glutamate Decarboxylase.
- enzymology : Vestibular Nuclei.
- innervation : Vestibule, Labyrinth.
- metabolism : Astrocytes, Neurons, Afferent.
- pathology : Aging, Astrocytes, Neurons, Afferent, Vestibular Nuclei, Vestibule, Labyrinth.
- physiology : Behavior, Animal, Recovery of Function.
- physiopathology : Vestibular Nuclei, Vestibule, Labyrinth.
- Animals, Cats, Cell Differentiation, Cell Proliferation, Cell Survival, Neurogenesis, Time Factors.
Abstract
Functional and reactive neurogenesis and astrogenesis are observed in deafferented vestibular nuclei after unilateral vestibular nerve section in adult cats. The newborn cells survive up to one month and contribute actively to the successful recovery of posturo-locomotor functions. This study investigates whether the nature of vestibular deafferentation has an incidence on the neurogenic potential of the vestibular nuclei, and on the time course of behavioural recovery. Three animal models that mimic different vestibular pathologies were used: unilateral and permanent suppression of vestibular input by unilateral vestibular neurectomy (UVN), or by unilateral labyrinthectomy (UL, the mechanical destruction of peripheral vestibular receptors), or unilateral and reversible blockade of vestibular nerve input using tetrodotoxin (TTX). Neurogenesis and astrogenesis were revealed in the vestibular nuclei using bromodeoxyuridine (BrdU) as a newborn cell marker, while glial fibrillary acidic protein (GFAP) and glutamate decarboxylase 67 (GAD67) were used to identify astrocytes and GABAergic neurons, respectively. Spontaneous nystagmus and posturo-locomotor tests (static and dynamic balance performance) were carried out to quantify the behavioural recovery process. Results showed that the nature of vestibular loss determined the cellular plastic events occurring in the vestibular nuclei and affected the time course of behavioural recovery. Interestingly, the deafferented vestibular nuclei express neurogenic potential after acute and total vestibular loss only (UVN), while non-structural plastic processes are involved when the vestibular deafferentation is less drastic (UL, TTX). This is the first experimental evidence that the vestibular complex in the brainstem can become neurogenic under specific injury. These new data are of interest for understanding the factors favouring the expression of functional neurogenesis in adult mammals in a brain repair perspective, and are of clinical relevance in vestibular pathology.
DOI: 10.1371/journal.pone.0022262
PubMed: 21853029
PubMed Central: PMC3154899
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Nuclei</term><term>Vestibule, Labyrinth</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cats</term><term>Cell Differentiation</term><term>Cell Proliferation</term><term>Cell Survival</term><term>Neurogenesis</term><term>Time Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Chats</term><term>Différenciation cellulaire</term><term>Facteurs temps</term><term>Neurogenèse</term><term>Prolifération cellulaire</term><term>Survie cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Functional and reactive neurogenesis and astrogenesis are observed in deafferented vestibular nuclei after unilateral vestibular nerve section in adult cats. The newborn cells survive up to one month and contribute actively to the successful recovery of posturo-locomotor functions. This study investigates whether the nature of vestibular deafferentation has an incidence on the neurogenic potential of the vestibular nuclei, and on the time course of behavioural recovery. Three animal models that mimic different vestibular pathologies were used: unilateral and permanent suppression of vestibular input by unilateral vestibular neurectomy (UVN), or by unilateral labyrinthectomy (UL, the mechanical destruction of peripheral vestibular receptors), or unilateral and reversible blockade of vestibular nerve input using tetrodotoxin (TTX). Neurogenesis and astrogenesis were revealed in the vestibular nuclei using bromodeoxyuridine (BrdU) as a newborn cell marker, while glial fibrillary acidic protein (GFAP) and glutamate decarboxylase 67 (GAD67) were used to identify astrocytes and GABAergic neurons, respectively. Spontaneous nystagmus and posturo-locomotor tests (static and dynamic balance performance) were carried out to quantify the behavioural recovery process. Results showed that the nature of vestibular loss determined the cellular plastic events occurring in the vestibular nuclei and affected the time course of behavioural recovery. Interestingly, the deafferented vestibular nuclei express neurogenic potential after acute and total vestibular loss only (UVN), while non-structural plastic processes are involved when the vestibular deafferentation is less drastic (UL, TTX). This is the first experimental evidence that the vestibular complex in the brainstem can become neurogenic under specific injury. These new data are of interest for understanding the factors favouring the expression of functional neurogenesis in adult mammals in a brain repair perspective, and are of clinical relevance in vestibular pathology.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21853029</PMID><DateCompleted><Year>2011</Year><Month>12</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>6</Volume><Issue>8</Issue><PubDate><Year>2011</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS One</ISOAbbreviation></Journal><ArticleTitle>Neurogenic potential of the vestibular nuclei and behavioural recovery time course in the adult cat are governed by the nature of the vestibular damage.</ArticleTitle><Pagination><MedlinePgn>e22262</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0022262</ELocationID><Abstract><AbstractText>Functional and reactive neurogenesis and astrogenesis are observed in deafferented vestibular nuclei after unilateral vestibular nerve section in adult cats. The newborn cells survive up to one month and contribute actively to the successful recovery of posturo-locomotor functions. This study investigates whether the nature of vestibular deafferentation has an incidence on the neurogenic potential of the vestibular nuclei, and on the time course of behavioural recovery. Three animal models that mimic different vestibular pathologies were used: unilateral and permanent suppression of vestibular input by unilateral vestibular neurectomy (UVN), or by unilateral labyrinthectomy (UL, the mechanical destruction of peripheral vestibular receptors), or unilateral and reversible blockade of vestibular nerve input using tetrodotoxin (TTX). Neurogenesis and astrogenesis were revealed in the vestibular nuclei using bromodeoxyuridine (BrdU) as a newborn cell marker, while glial fibrillary acidic protein (GFAP) and glutamate decarboxylase 67 (GAD67) were used to identify astrocytes and GABAergic neurons, respectively. Spontaneous nystagmus and posturo-locomotor tests (static and dynamic balance performance) were carried out to quantify the behavioural recovery process. Results showed that the nature of vestibular loss determined the cellular plastic events occurring in the vestibular nuclei and affected the time course of behavioural recovery. Interestingly, the deafferented vestibular nuclei express neurogenic potential after acute and total vestibular loss only (UVN), while non-structural plastic processes are involved when the vestibular deafferentation is less drastic (UL, TTX). This is the first experimental evidence that the vestibular complex in the brainstem can become neurogenic under specific injury. These new data are of interest for understanding the factors favouring the expression of functional neurogenesis in adult mammals in a brain repair perspective, and are of clinical relevance in vestibular pathology.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dutheil</LastName><ForeName>Sophie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Département de Neurosciences, UMR 6149 Neurosciences Intégratives et Adaptatives, Université de Provence/CNRS-Pôle 3C (Comportement, Cerveau, Cognition), Centre de Saint Charles, Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lacour</LastName><ForeName>Michel</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Tighilet</LastName><ForeName>Brahim</ForeName><Initials>B</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType 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MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001253" MajorTopicYN="N">Astrocytes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001522" MajorTopicYN="N">Behavior, Animal</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002415" MajorTopicYN="N">Cats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005904" MajorTopicYN="N">Glial Fibrillary Acidic Protein</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005968" MajorTopicYN="N">Glutamate Decarboxylase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055495" MajorTopicYN="Y">Neurogenesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009475" MajorTopicYN="N">Neurons, Afferent</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020127" MajorTopicYN="N">Recovery of Function</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014726" MajorTopicYN="N">Vestibular Nuclei</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014722" MajorTopicYN="N">Vestibule, Labyrinth</DescriptorName><QualifierName UI="Q000294" MajorTopicYN="Y">innervation</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2011</Year><Month>01</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>06</Month><Day>22</Day></PubMedPubDate><PubMedPubDate 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