Bee Venom Alleviates Motor Deficits and Modulates the Transfer of Cortical Information through the Basal Ganglia in Rat Models of Parkinson's Disease.
Identifieur interne : 000407 ( PubMed/Checkpoint ); précédent : 000406; suivant : 000408Bee Venom Alleviates Motor Deficits and Modulates the Transfer of Cortical Information through the Basal Ganglia in Rat Models of Parkinson's Disease.
Auteurs : Nicolas Maurice [France] ; Thierry Deltheil [France] ; Christophe Melon [France] ; Bertrand Degos [France] ; Christiane Mourre [France] ; Marianne Amalric [France] ; Lydia Kerkerian-Le Goff [France]Source :
- PloS one [ 1932-6203 ] ; 2015.
English descriptors
- KwdEn :
- Action Potentials (drug effects), Animals, Basal Ganglia (drug effects), Basal Ganglia (physiopathology), Bee Venoms (administration & dosage), Bee Venoms (pharmacology), Bee Venoms (therapeutic use), Catalepsy (complications), Catalepsy (drug therapy), Catalepsy (physiopathology), Disease Models, Animal, Dopamine Antagonists (pharmacology), Electric Stimulation, Haloperidol, Male, Motor Activity (drug effects), Motor Cortex (drug effects), Motor Cortex (physiopathology), Oxidopamine, Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Rats, Wistar, Receptors, Dopamine (metabolism), Substantia Nigra (drug effects), Substantia Nigra (physiopathology).
- MESH :
- chemical , administration & dosage : Bee Venoms.
- complications : Catalepsy, Parkinson Disease.
- drug effects : Action Potentials, Basal Ganglia, Motor Activity, Motor Cortex, Substantia Nigra.
- drug therapy : Catalepsy, Parkinson Disease.
- chemical , metabolism : Receptors, Dopamine.
- chemical , pharmacology : Bee Venoms, Dopamine Antagonists.
- physiopathology : Basal Ganglia, Catalepsy, Motor Cortex, Parkinson Disease, Substantia Nigra.
- chemical , therapeutic use : Bee Venoms.
- Animals, Disease Models, Animal, Electric Stimulation, Haloperidol, Male, Oxidopamine, Rats, Wistar.
Abstract
Recent evidence points to a neuroprotective action of bee venom on nigral dopamine neurons in animal models of Parkinson's disease (PD). Here we examined whether bee venom also displays a symptomatic action by acting on the pathological functioning of the basal ganglia in rat PD models. Bee venom effects were assessed by combining motor behavior analyses and in vivo electrophysiological recordings in the substantia nigra pars reticulata (SNr, basal ganglia output structure) in pharmacological (neuroleptic treatment) and lesional (unilateral intranigral 6-hydroxydopamine injection) PD models. In the hemi-parkinsonian 6-hydroxydopamine lesion model, subchronic bee venom treatment significantly alleviates contralateral forelimb akinesia and apomorphine-induced rotations. Moreover, a single injection of bee venom reverses haloperidol-induced catalepsy, a pharmacological model reminiscent of parkinsonian akinetic deficit. This effect is mimicked by apamin, a blocker of small conductance Ca2+-activated K+ (SK) channels, and blocked by CyPPA, a positive modulator of these channels, suggesting the involvement of SK channels in the bee venom antiparkinsonian action. In vivo electrophysiological recordings in the substantia nigra pars reticulata (basal ganglia output structure) showed no significant effect of BV on the mean neuronal discharge frequency or pathological bursting activity. In contrast, analyses of the neuronal responses evoked by motor cortex stimulation show that bee venom reverses the 6-OHDA- and neuroleptic-induced biases in the influence exerted by the direct inhibitory and indirect excitatory striatonigral circuits. These data provide the first evidence for a beneficial action of bee venom on the pathological functioning of the cortico-basal ganglia circuits underlying motor PD symptoms with potential relevance to the symptomatic treatment of this disease.
DOI: 10.1371/journal.pone.0142838
PubMed: 26571268
Affiliations:
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(administration & dosage)</term><term>Bee Venoms (pharmacology)</term><term>Bee Venoms (therapeutic use)</term><term>Catalepsy (complications)</term><term>Catalepsy (drug therapy)</term><term>Catalepsy (physiopathology)</term><term>Disease Models, Animal</term><term>Dopamine Antagonists (pharmacology)</term><term>Electric Stimulation</term><term>Haloperidol</term><term>Male</term><term>Motor Activity (drug effects)</term><term>Motor Cortex (drug effects)</term><term>Motor Cortex (physiopathology)</term><term>Oxidopamine</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Rats, Wistar</term><term>Receptors, Dopamine (metabolism)</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Bee Venoms</term></keywords><keywords scheme="MESH" 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Here we examined whether bee venom also displays a symptomatic action by acting on the pathological functioning of the basal ganglia in rat PD models. Bee venom effects were assessed by combining motor behavior analyses and in vivo electrophysiological recordings in the substantia nigra pars reticulata (SNr, basal ganglia output structure) in pharmacological (neuroleptic treatment) and lesional (unilateral intranigral 6-hydroxydopamine injection) PD models. In the hemi-parkinsonian 6-hydroxydopamine lesion model, subchronic bee venom treatment significantly alleviates contralateral forelimb akinesia and apomorphine-induced rotations. Moreover, a single injection of bee venom reverses haloperidol-induced catalepsy, a pharmacological model reminiscent of parkinsonian akinetic deficit. This effect is mimicked by apamin, a blocker of small conductance Ca2+-activated K+ (SK) channels, and blocked by CyPPA, a positive modulator of these channels, suggesting the involvement of SK channels in the bee venom antiparkinsonian action. In vivo electrophysiological recordings in the substantia nigra pars reticulata (basal ganglia output structure) showed no significant effect of BV on the mean neuronal discharge frequency or pathological bursting activity. In contrast, analyses of the neuronal responses evoked by motor cortex stimulation show that bee venom reverses the 6-OHDA- and neuroleptic-induced biases in the influence exerted by the direct inhibitory and indirect excitatory striatonigral circuits. These data provide the first evidence for a beneficial action of bee venom on the pathological functioning of the cortico-basal ganglia circuits underlying motor PD symptoms with potential relevance to the symptomatic treatment of this disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26571268</PMID><DateCreated><Year>2015</Year><Month>11</Month><Day>17</Day></DateCreated><DateCompleted><Year>2016</Year><Month>06</Month><Day>21</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>15</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>11</Issue><PubDate><Year>2015</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Bee Venom Alleviates Motor Deficits and Modulates the Transfer of Cortical Information through the Basal Ganglia in Rat Models of Parkinson's Disease.</ArticleTitle><Pagination><MedlinePgn>e0142838</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0142838</ELocationID><Abstract><AbstractText>Recent evidence points to a neuroprotective action of bee venom on nigral dopamine neurons in animal models of Parkinson's disease (PD). Here we examined whether bee venom also displays a symptomatic action by acting on the pathological functioning of the basal ganglia in rat PD models. Bee venom effects were assessed by combining motor behavior analyses and in vivo electrophysiological recordings in the substantia nigra pars reticulata (SNr, basal ganglia output structure) in pharmacological (neuroleptic treatment) and lesional (unilateral intranigral 6-hydroxydopamine injection) PD models. In the hemi-parkinsonian 6-hydroxydopamine lesion model, subchronic bee venom treatment significantly alleviates contralateral forelimb akinesia and apomorphine-induced rotations. Moreover, a single injection of bee venom reverses haloperidol-induced catalepsy, a pharmacological model reminiscent of parkinsonian akinetic deficit. This effect is mimicked by apamin, a blocker of small conductance Ca2+-activated K+ (SK) channels, and blocked by CyPPA, a positive modulator of these channels, suggesting the involvement of SK channels in the bee venom antiparkinsonian action. In vivo electrophysiological recordings in the substantia nigra pars reticulata (basal ganglia output structure) showed no significant effect of BV on the mean neuronal discharge frequency or pathological bursting activity. In contrast, analyses of the neuronal responses evoked by motor cortex stimulation show that bee venom reverses the 6-OHDA- and neuroleptic-induced biases in the influence exerted by the direct inhibitory and indirect excitatory striatonigral circuits. These data provide the first evidence for a beneficial action of bee venom on the pathological functioning of the cortico-basal ganglia circuits underlying motor PD symptoms with potential relevance to the symptomatic treatment of this disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Maurice</LastName><ForeName>Nicolas</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Aix Marseille Université, CNRS, IBDM UMR 7288, Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deltheil</LastName><ForeName>Thierry</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Aix Marseille Université, CNRS, LNC UMR 7291, Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Melon</LastName><ForeName>Christophe</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Aix Marseille Université, CNRS, IBDM UMR 7288, Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Degos</LastName><ForeName>Bertrand</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>INSERM, CNRS, Collège de France, CIRB UMR 7241 U-1050, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>APHP, Département des Maladies du Système Nerveux, Centre Expert Inter-Régional Ile de France de la Maladie de Parkinson, Hôpital Pitié-Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mourre</LastName><ForeName>Christiane</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Aix Marseille Université, CNRS, LNC UMR 7291, Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Amalric</LastName><ForeName>Marianne</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Aix Marseille Université, CNRS, LNC UMR 7291, Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kerkerian-Le Goff</LastName><ForeName>Lydia</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Aix Marseille Université, CNRS, IBDM UMR 7288, Marseille, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>ClinicalTrials.gov</DataBankName><AccessionNumberList><AccessionNumber>NCT01341431</AccessionNumber></AccessionNumberList></DataBank></DataBankList><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>11</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS 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Version="1">9457173</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="N">Action Potentials</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001479" MajorTopicYN="N">Basal Ganglia</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001514" MajorTopicYN="N">Bee Venoms</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002375" 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MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4646345</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>07</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>10</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>11</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>11</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>6</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26571268</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0142838</ArticleId><ArticleId IdType="pii">PONE-D-15-32902</ArticleId><ArticleId IdType="pmc">PMC4646345</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Provence-Alpes-Côte d'Azur</li><li>Île-de-France</li></region><settlement><li>Marseille</li><li>Paris</li></settlement><orgName><li>Université d'Aix-Marseille</li></orgName></list><tree><country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Maurice, Nicolas" sort="Maurice, Nicolas" uniqKey="Maurice N" first="Nicolas" last="Maurice">Nicolas Maurice</name></region><name sortKey="Amalric, Marianne" sort="Amalric, Marianne" uniqKey="Amalric M" first="Marianne" last="Amalric">Marianne Amalric</name><name sortKey="Degos, Bertrand" sort="Degos, Bertrand" uniqKey="Degos B" first="Bertrand" last="Degos">Bertrand Degos</name><name sortKey="Deltheil, Thierry" sort="Deltheil, Thierry" uniqKey="Deltheil T" first="Thierry" last="Deltheil">Thierry Deltheil</name><name sortKey="Kerkerian Le Goff, Lydia" sort="Kerkerian Le Goff, Lydia" uniqKey="Kerkerian Le Goff L" first="Lydia" last="Kerkerian-Le Goff">Lydia Kerkerian-Le Goff</name><name sortKey="Melon, Christophe" sort="Melon, Christophe" uniqKey="Melon C" first="Christophe" last="Melon">Christophe Melon</name><name sortKey="Mourre, Christiane" sort="Mourre, Christiane" uniqKey="Mourre C" first="Christiane" last="Mourre">Christiane Mourre</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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