ParkinsonCanadaV1, Main, Exploration, bibRecord, 002915

Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease

Identifieur interne : 002915 ( Main/Exploration ); précédent : 002914; suivant : 002916

Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease

Auteurs : Rohita Sharma [Canada] ; Catherine R. Mcmillan [Canada] ; Catherine C. Tenn [Canada] ; Lennard P. Niles [Canada]

Source :

Brain research [ 0006-8993 ] ; 2006.

RBID : Pascal:06-0132091

Descripteurs français

Pascal (Inist)
- Neuroprotection, Mélatonine, Oxidopamine, Modèle, Lésion, Corps strié, Tyrosine 3-monooxygenase, Facteur GDNF, Parkinson maladie, Facteur BDNF, Rat, Animal.

English descriptors

KwdEn :
- Animal, Animals, Apomorphine (antagonists & inhibitors), Apomorphine (pharmacology), Brain derived neurotrophic factor, Brain-Derived Neurotrophic Factor (biosynthesis), Brain-Derived Neurotrophic Factor (genetics), Corpus striatum, Densitometry, Dopamine Agonists (pharmacology), Functional Laterality (physiology), Glial Cell Line-Derived Neurotrophic Factor (biosynthesis), Glial Cell Line-Derived Neurotrophic Factor (genetics), Glial cell line derived neurotrophic factor, Immunohistochemistry, Lesion, Male, Melatonin, Melatonin (pharmacology), Models, Neostriatum (drug effects), Neostriatum (enzymology), Neuroprotection, Neuroprotective Agents, Oxidopamine, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (prevention & control), Parkinson disease, RNA, Messenger (biosynthesis), Rat, Rats, Rats, Sprague-Dawley, Receptor, Melatonin, MT1 (drug effects), Receptors, Melatonin (drug effects), Reverse Transcriptase Polymerase Chain Reaction, Stereotyped Behavior (drug effects), Sympatholytics, Tyrosine 3-Monooxygenase (metabolism), Tyrosine 3-monooxygenase.
MESH :
- chemical , antagonists & inhibitors : Apomorphine.
- chemical , biosynthesis : Brain-Derived Neurotrophic Factor, Glial Cell Line-Derived Neurotrophic Factor, RNA, Messenger.
- chemical , drug effects : Receptor, Melatonin, MT1, Receptors, Melatonin.
- chemical , genetics : Brain-Derived Neurotrophic Factor, Glial Cell Line-Derived Neurotrophic Factor.
- chemical , metabolism : Tyrosine 3-Monooxygenase.
- chemical , pharmacology : Apomorphine, Dopamine Agonists, Melatonin.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Neostriatum, Stereotyped Behavior.
- enzymology : Neostriatum.
- physiology : Functional Laterality.
- prevention & control : Parkinson Disease, Secondary.
- Animals, Densitometry, Immunohistochemistry, Male, Neuroprotective Agents, Oxidopamine, Rats, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction, Sympatholytics.

Abstract

There is considerable evidence that pharmacological doses of the pineal hormone, melatonin, are neuroprotective in diverse models of neurodegeneration including Parkinson's disease. However, there is limited information about the effects of physiological doses of this hormone in similar models. In this study, rats were chronically treated with melatonin via drinking water following partial 6-hydroxydopamine lesioning in the striatum. The two doses of melatonin (0.4 μg/ml and 4.0 μg/ml) were within the reported physiological concentrations present in the serum and cerebrospinal fluid respectively. At 2 weeks after surgery, the higher dose of melatonin significantly attenuated rotational behavior in hemi-parkinsonian rats compared to similarly lesioned animals receiving either vehicle (P < 0.001) or the lower dose of melatonin (P < 0.01). Animals were perfused or sacrificed 10 weeks after commencing melatonin treatment for immunohistochemical or mRNA studies. Animals treated with 4.0 pg/ml melatonin exhibited normal tyrosine hydroxylase (TH) immunoreactivity in the lesioned striatum, whereas little or no TH immunofluorescence was visible in similarly lesioned animals receiving vehicle. In contrast, semiquantitative RT-PCR analysis revealed no group differences in TH mRNA, suggesting spontaneous recovery of this transcript as observed previously in partially lesioned animals. There were no significant differences in striatal GDNF mRNA levels between sham and lesioned animals. However, there was a significant (P < 0.01) increase in GDNF mRNA expression in the intact contralateral striata of lesioned animals treated with vehicle. Interestingly, melatonin treatment attenuated this novel compensatory contralateral increase in striatal GDNF expression, presumably due to its neuroprotective effect. These findings support a physiological role for melatonin in protecting against parkinsonian neurodegeneration in the nigrostriatal system.

Affiliations:

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease</title>
<author><name sortKey="Sharma, Rohita" sort="Sharma, Rohita" uniqKey="Sharma R" first="Rohita" last="Sharma">Rohita Sharma</name>
<affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West</s1>
<s2>Hamilton, Ontario, L8N 3Z5</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
<country>Canada</country>
<wicri:noRegion>Hamilton, Ontario, L8N 3Z5</wicri:noRegion>
<orgName type="university">Université McMaster</orgName>
<placeName><settlement type="city">Hamilton (Ontario)</settlement>
<region type="state">Ontario</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Mcmillan, Catherine R" sort="Mcmillan, Catherine R" uniqKey="Mcmillan C" first="Catherine R." last="Mcmillan">Catherine R. Mcmillan</name>
<affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West</s1>
<s2>Hamilton, Ontario, L8N 3Z5</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
<country>Canada</country>
<wicri:noRegion>Hamilton, Ontario, L8N 3Z5</wicri:noRegion>
<orgName type="university">Université McMaster</orgName>
<placeName><settlement type="city">Hamilton (Ontario)</settlement>
<region type="state">Ontario</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tenn, Catherine C" sort="Tenn, Catherine C" uniqKey="Tenn C" first="Catherine C." last="Tenn">Catherine C. Tenn</name>
<affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Schizophrenia/PET Centre, Centre for Addiction and Mental Health</s1>
<s2>Toronto, Ontario</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
<country>Canada</country>
<wicri:noRegion>Toronto, Ontario</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Niles, Lennard P" sort="Niles, Lennard P" uniqKey="Niles L" first="Lennard P." last="Niles">Lennard P. Niles</name>
<affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West</s1>
<s2>Hamilton, Ontario, L8N 3Z5</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
<country>Canada</country>
<wicri:noRegion>Hamilton, Ontario, L8N 3Z5</wicri:noRegion>
<orgName type="university">Université McMaster</orgName>
<placeName><settlement type="city">Hamilton (Ontario)</settlement>
<region type="state">Ontario</region>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">06-0132091</idno>
<date when="2006">2006</date>
<idno type="stanalyst">PASCAL 06-0132091 INIST</idno>
<idno type="RBID">Pascal:06-0132091</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000860</idno>
<idno type="wicri:Area/PascalFrancis/Curation">000463</idno>
<idno type="wicri:Area/PascalFrancis/Checkpoint">000709</idno>
<idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000709</idno>
<idno type="wicri:doubleKey">0006-8993:2006:Sharma R:physiological:neuroprotection:by</idno>
<idno type="wicri:Area/Main/Merge">002C07</idno>
<idno type="wicri:source">PubMed</idno>
<idno type="RBID">pubmed:16375867</idno>
<idno type="wicri:Area/PubMed/Corpus">001194</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001194</idno>
<idno type="wicri:Area/PubMed/Curation">001194</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001194</idno>
<idno type="wicri:Area/PubMed/Checkpoint">001194</idno>
<idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001194</idno>
<idno type="wicri:Area/Ncbi/Merge">000600</idno>
<idno type="wicri:Area/Ncbi/Curation">000600</idno>
<idno type="wicri:Area/Ncbi/Checkpoint">000600</idno>
<idno type="wicri:doubleKey">0006-8993:2006:Sharma R:physiological:neuroprotection:by</idno>
<idno type="wicri:Area/Main/Merge">002A00</idno>
<idno type="wicri:Area/Main/Curation">002915</idno>
<idno type="wicri:Area/Main/Exploration">002915</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease</title>
<author><name sortKey="Sharma, Rohita" sort="Sharma, Rohita" uniqKey="Sharma R" first="Rohita" last="Sharma">Rohita Sharma</name>
<affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West</s1>
<s2>Hamilton, Ontario, L8N 3Z5</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
<country>Canada</country>
<wicri:noRegion>Hamilton, Ontario, L8N 3Z5</wicri:noRegion>
<orgName type="university">Université McMaster</orgName>
<placeName><settlement type="city">Hamilton (Ontario)</settlement>
<region type="state">Ontario</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Mcmillan, Catherine R" sort="Mcmillan, Catherine R" uniqKey="Mcmillan C" first="Catherine R." last="Mcmillan">Catherine R. Mcmillan</name>
<affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West</s1>
<s2>Hamilton, Ontario, L8N 3Z5</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
<country>Canada</country>
<wicri:noRegion>Hamilton, Ontario, L8N 3Z5</wicri:noRegion>
<orgName type="university">Université McMaster</orgName>
<placeName><settlement type="city">Hamilton (Ontario)</settlement>
<region type="state">Ontario</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tenn, Catherine C" sort="Tenn, Catherine C" uniqKey="Tenn C" first="Catherine C." last="Tenn">Catherine C. Tenn</name>
<affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Schizophrenia/PET Centre, Centre for Addiction and Mental Health</s1>
<s2>Toronto, Ontario</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
<country>Canada</country>
<wicri:noRegion>Toronto, Ontario</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Niles, Lennard P" sort="Niles, Lennard P" uniqKey="Niles L" first="Lennard P." last="Niles">Lennard P. Niles</name>
<affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main Street West</s1>
<s2>Hamilton, Ontario, L8N 3Z5</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
</inist:fA14>
<country>Canada</country>
<wicri:noRegion>Hamilton, Ontario, L8N 3Z5</wicri:noRegion>
<orgName type="university">Université McMaster</orgName>
<placeName><settlement type="city">Hamilton (Ontario)</settlement>
<region type="state">Ontario</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Brain research</title>
<title level="j" type="abbreviated">Brain res.</title>
<idno type="ISSN">0006-8993</idno>
<imprint><date when="2006">2006</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Brain research</title>
<title level="j" type="abbreviated">Brain res.</title>
<idno type="ISSN">0006-8993</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term>
<term>Animals</term>
<term>Apomorphine (antagonists & inhibitors)</term>
<term>Apomorphine (pharmacology)</term>
<term>Brain derived neurotrophic factor</term>
<term>Brain-Derived Neurotrophic Factor (biosynthesis)</term>
<term>Brain-Derived Neurotrophic Factor (genetics)</term>
<term>Corpus striatum</term>
<term>Densitometry</term>
<term>Dopamine Agonists (pharmacology)</term>
<term>Functional Laterality (physiology)</term>
<term>Glial Cell Line-Derived Neurotrophic Factor (biosynthesis)</term>
<term>Glial Cell Line-Derived Neurotrophic Factor (genetics)</term>
<term>Glial cell line derived neurotrophic factor</term>
<term>Immunohistochemistry</term>
<term>Lesion</term>
<term>Male</term>
<term>Melatonin</term>
<term>Melatonin (pharmacology)</term>
<term>Models</term>
<term>Neostriatum (drug effects)</term>
<term>Neostriatum (enzymology)</term>
<term>Neuroprotection</term>
<term>Neuroprotective Agents</term>
<term>Oxidopamine</term>
<term>Parkinson Disease, Secondary (chemically induced)</term>
<term>Parkinson Disease, Secondary (prevention & control)</term>
<term>Parkinson disease</term>
<term>RNA, Messenger (biosynthesis)</term>
<term>Rat</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Receptor, Melatonin, MT1 (drug effects)</term>
<term>Receptors, Melatonin (drug effects)</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>Stereotyped Behavior (drug effects)</term>
<term>Sympatholytics</term>
<term>Tyrosine 3-Monooxygenase (metabolism)</term>
<term>Tyrosine 3-monooxygenase</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Apomorphine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Brain-Derived Neurotrophic Factor</term>
<term>Glial Cell Line-Derived Neurotrophic Factor</term>
<term>RNA, Messenger</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptor, Melatonin, MT1</term>
<term>Receptors, Melatonin</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Brain-Derived Neurotrophic Factor</term>
<term>Glial Cell Line-Derived Neurotrophic Factor</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Apomorphine</term>
<term>Dopamine Agonists</term>
<term>Melatonin</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Neostriatum</term>
<term>Stereotyped Behavior</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Neostriatum</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Functional Laterality</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Parkinson Disease, Secondary</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Densitometry</term>
<term>Immunohistochemistry</term>
<term>Male</term>
<term>Neuroprotective Agents</term>
<term>Oxidopamine</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>Sympatholytics</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Neuroprotection</term>
<term>Mélatonine</term>
<term>Oxidopamine</term>
<term>Modèle</term>
<term>Lésion</term>
<term>Corps strié</term>
<term>Tyrosine 3-monooxygenase</term>
<term>Facteur GDNF</term>
<term>Parkinson maladie</term>
<term>Facteur BDNF</term>
<term>Rat</term>
<term>Animal</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">There is considerable evidence that pharmacological doses of the pineal hormone, melatonin, are neuroprotective in diverse models of neurodegeneration including Parkinson's disease. However, there is limited information about the effects of physiological doses of this hormone in similar models. In this study, rats were chronically treated with melatonin via drinking water following partial 6-hydroxydopamine lesioning in the striatum. The two doses of melatonin (0.4 μg/ml and 4.0 μg/ml) were within the reported physiological concentrations present in the serum and cerebrospinal fluid respectively. At 2 weeks after surgery, the higher dose of melatonin significantly attenuated rotational behavior in hemi-parkinsonian rats compared to similarly lesioned animals receiving either vehicle (P < 0.001) or the lower dose of melatonin (P < 0.01). Animals were perfused or sacrificed 10 weeks after commencing melatonin treatment for immunohistochemical or mRNA studies. Animals treated with 4.0 pg/ml melatonin exhibited normal tyrosine hydroxylase (TH) immunoreactivity in the lesioned striatum, whereas little or no TH immunofluorescence was visible in similarly lesioned animals receiving vehicle. In contrast, semiquantitative RT-PCR analysis revealed no group differences in TH mRNA, suggesting spontaneous recovery of this transcript as observed previously in partially lesioned animals. There were no significant differences in striatal GDNF mRNA levels between sham and lesioned animals. However, there was a significant (P < 0.01) increase in GDNF mRNA expression in the intact contralateral striata of lesioned animals treated with vehicle. Interestingly, melatonin treatment attenuated this novel compensatory contralateral increase in striatal GDNF expression, presumably due to its neuroprotective effect. These findings support a physiological role for melatonin in protecting against parkinsonian neurodegeneration in the nigrostriatal system.</div>
</front>
</TEI>
<affiliations><list><country><li>Canada</li>
</country>
<region><li>Ontario</li>
</region>
<settlement><li>Hamilton (Ontario)</li>
</settlement>
<orgName><li>Université McMaster</li>
</orgName>
</list>
<tree><country name="Canada"><region name="Ontario"><name sortKey="Sharma, Rohita" sort="Sharma, Rohita" uniqKey="Sharma R" first="Rohita" last="Sharma">Rohita Sharma</name>
</region>
<name sortKey="Mcmillan, Catherine R" sort="Mcmillan, Catherine R" uniqKey="Mcmillan C" first="Catherine R." last="Mcmillan">Catherine R. Mcmillan</name>
<name sortKey="Niles, Lennard P" sort="Niles, Lennard P" uniqKey="Niles L" first="Lennard P." last="Niles">Lennard P. Niles</name>
<name sortKey="Tenn, Catherine C" sort="Tenn, Catherine C" uniqKey="Tenn C" first="Catherine C." last="Tenn">Catherine C. Tenn</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002915 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 002915 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Canada
   |area=    ParkinsonCanadaV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     Pascal:06-0132091
   |texte=   Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease
}}

This area was generated with Dilib version V0.6.29.
Data generation: Thu May 4 22:20:19 2017. Site generation: Fri Dec 23 23:17:26 2022

La maladie de Parkinson au Canada (serveur d'exploration)

Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease

Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

	La maladie de Parkinson au Canada (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.