The combined depletion of monoamines alters the effectiveness of subthalamic deep brain stimulation.
Identifieur interne : 000288 ( PubMed/Corpus ); précédent : 000287; suivant : 000289The combined depletion of monoamines alters the effectiveness of subthalamic deep brain stimulation.
Auteurs : Emilie Faggiani ; Claire Delaville ; Abdelhamid BenazzouzSource :
- Neurobiology of disease [ 1095-953X ] ; 2015.
English descriptors
- KwdEn :
- Animals, Anxiety Disorders (physiopathology), Anxiety Disorders (therapy), Benzylamines, Biogenic Monoamines (metabolism), Catalepsy (physiopathology), Catalepsy (therapy), Corpus Striatum (metabolism), Deep Brain Stimulation (methods), Depressive Disorder (physiopathology), Depressive Disorder (therapy), Dopamine (deficiency), Frontal Lobe (metabolism), Male, Motor Activity (physiology), Oxidopamine, Parkinsonian Disorders (physiopathology), Parkinsonian Disorders (psychology), Parkinsonian Disorders (therapy), Rats, Sprague-Dawley, Subthalamic Nucleus (metabolism).
- MESH :
- chemical , deficiency : Dopamine.
- chemical , metabolism : Biogenic Monoamines.
- chemical : Benzylamines, Oxidopamine.
- metabolism : Corpus Striatum, Frontal Lobe, Subthalamic Nucleus.
- methods : Deep Brain Stimulation.
- physiology : Motor Activity.
- physiopathology : Anxiety Disorders, Catalepsy, Depressive Disorder, Parkinsonian Disorders.
- psychology : Parkinsonian Disorders.
- therapy : Anxiety Disorders, Catalepsy, Depressive Disorder, Parkinsonian Disorders.
- Animals, Male, Rats, Sprague-Dawley.
Abstract
Non-motor symptoms of Parkinson's disease are under-studied and therefore not well treated. Here, we investigated the role of combined depletions of dopamine, norepinephrine and/or serotonin in the manifestation of motor and non-motor deficits in the rat. Then, we studied the impact of these depletions on the efficacy of deep brain stimulation of the subthalamic nucleus (STN-DBS). We performed selective depletions of dopamine, norepinephrine and serotonin, and the behavioral effects of different combined depletions were investigated using the open field, the elevated plus maze and the forced swim test. Bilateral dopamine depletion alone induced locomotor deficits associated with anxiety and mild "depressive-like" behaviors. Although additional depletions of norepinephrine and/or serotonin did not potentiate locomotor and anxiety disorders, combined depletions of the three monoamines dramatically exacerbated "depressive-like" behavior. STN-DBS markedly reversed locomotor deficits and anxiety behavior in animals with bilateral dopamine depletion alone. However, these improvements were reduced or lost by the additional depletion of norepinephrine and/or serotonin, indicating that the depletion of these monoamines may interfere with the antiparkinsonian efficacy of STN-DBS. Furthermore, our results showed that acute STN-DBS improved "depressive-like" disorder in animals with bilateral depletion of dopamine and also in animals with combined depletions of the three monoamines, which induced severe immobility in the forced swim test. Our data highlight the key role of monoamine depletions in the pathophysiology of anxiety and depressive-like disorders and provide the first evidence of their negative consequences on the efficacy of STN-DBS upon the motor and anxiety disorders in the context of Parkinson's disease.
DOI: 10.1016/j.nbd.2015.07.010
PubMed: 26206409
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pubmed:26206409Le document en format XML
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Electronic address: abdelhamid.benazzouz@u-bordeaux.fr.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Neurobiology of disease</title><idno type="eISSN">1095-953X</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Anxiety Disorders (physiopathology)</term><term>Anxiety Disorders (therapy)</term><term>Benzylamines</term><term>Biogenic Monoamines (metabolism)</term><term>Catalepsy (physiopathology)</term><term>Catalepsy (therapy)</term><term>Corpus Striatum (metabolism)</term><term>Deep Brain Stimulation (methods)</term><term>Depressive Disorder (physiopathology)</term><term>Depressive Disorder (therapy)</term><term>Dopamine (deficiency)</term><term>Frontal Lobe (metabolism)</term><term>Male</term><term>Motor Activity (physiology)</term><term>Oxidopamine</term><term>Parkinsonian Disorders (physiopathology)</term><term>Parkinsonian Disorders (psychology)</term><term>Parkinsonian Disorders (therapy)</term><term>Rats, Sprague-Dawley</term><term>Subthalamic Nucleus (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biogenic Monoamines</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Benzylamines</term><term>Oxidopamine</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Frontal Lobe</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Deep Brain Stimulation</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Anxiety Disorders</term><term>Catalepsy</term><term>Depressive Disorder</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Anxiety Disorders</term><term>Catalepsy</term><term>Depressive Disorder</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Male</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Non-motor symptoms of Parkinson's disease are under-studied and therefore not well treated. Here, we investigated the role of combined depletions of dopamine, norepinephrine and/or serotonin in the manifestation of motor and non-motor deficits in the rat. Then, we studied the impact of these depletions on the efficacy of deep brain stimulation of the subthalamic nucleus (STN-DBS). We performed selective depletions of dopamine, norepinephrine and serotonin, and the behavioral effects of different combined depletions were investigated using the open field, the elevated plus maze and the forced swim test. Bilateral dopamine depletion alone induced locomotor deficits associated with anxiety and mild "depressive-like" behaviors. Although additional depletions of norepinephrine and/or serotonin did not potentiate locomotor and anxiety disorders, combined depletions of the three monoamines dramatically exacerbated "depressive-like" behavior. STN-DBS markedly reversed locomotor deficits and anxiety behavior in animals with bilateral dopamine depletion alone. However, these improvements were reduced or lost by the additional depletion of norepinephrine and/or serotonin, indicating that the depletion of these monoamines may interfere with the antiparkinsonian efficacy of STN-DBS. Furthermore, our results showed that acute STN-DBS improved "depressive-like" disorder in animals with bilateral depletion of dopamine and also in animals with combined depletions of the three monoamines, which induced severe immobility in the forced swim test. Our data highlight the key role of monoamine depletions in the pathophysiology of anxiety and depressive-like disorders and provide the first evidence of their negative consequences on the efficacy of STN-DBS upon the motor and anxiety disorders in the context of Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26206409</PMID><DateCreated><Year>2015</Year><Month>11</Month><Day>09</Day></DateCreated><DateCompleted><Year>2016</Year><Month>08</Month><Day>24</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-953X</ISSN><JournalIssue CitedMedium="Internet"><Volume>82</Volume><PubDate><Year>2015</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Neurobiology of disease</Title><ISOAbbreviation>Neurobiol. Dis.</ISOAbbreviation></Journal><ArticleTitle>The combined depletion of monoamines alters the effectiveness of subthalamic deep brain stimulation.</ArticleTitle><Pagination><MedlinePgn>342-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.nbd.2015.07.010</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0969-9961(15)30014-0</ELocationID><Abstract><AbstractText>Non-motor symptoms of Parkinson's disease are under-studied and therefore not well treated. Here, we investigated the role of combined depletions of dopamine, norepinephrine and/or serotonin in the manifestation of motor and non-motor deficits in the rat. Then, we studied the impact of these depletions on the efficacy of deep brain stimulation of the subthalamic nucleus (STN-DBS). We performed selective depletions of dopamine, norepinephrine and serotonin, and the behavioral effects of different combined depletions were investigated using the open field, the elevated plus maze and the forced swim test. Bilateral dopamine depletion alone induced locomotor deficits associated with anxiety and mild "depressive-like" behaviors. Although additional depletions of norepinephrine and/or serotonin did not potentiate locomotor and anxiety disorders, combined depletions of the three monoamines dramatically exacerbated "depressive-like" behavior. STN-DBS markedly reversed locomotor deficits and anxiety behavior in animals with bilateral dopamine depletion alone. However, these improvements were reduced or lost by the additional depletion of norepinephrine and/or serotonin, indicating that the depletion of these monoamines may interfere with the antiparkinsonian efficacy of STN-DBS. Furthermore, our results showed that acute STN-DBS improved "depressive-like" disorder in animals with bilateral depletion of dopamine and also in animals with combined depletions of the three monoamines, which induced severe immobility in the forced swim test. Our data highlight the key role of monoamine depletions in the pathophysiology of anxiety and depressive-like disorders and provide the first evidence of their negative consequences on the efficacy of STN-DBS upon the motor and anxiety disorders in the context of Parkinson's disease.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Faggiani</LastName><ForeName>Emilie</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, 33076 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, 33076 Bordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delaville</LastName><ForeName>Claire</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, 33076 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, 33076 Bordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Benazzouz</LastName><ForeName>Abdelhamid</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, 33076 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, 33076 Bordeaux, France. Electronic address: abdelhamid.benazzouz@u-bordeaux.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>07</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Dis</MedlineTA><NlmUniqueID>9500169</NlmUniqueID><ISSNLinking>0969-9961</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001596">Benzylamines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015306">Biogenic Monoamines</NameOfSubstance></Chemical><Chemical><RegistryNumber>8HW4YBZ748</RegistryNumber><NameOfSubstance 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