Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease
Identifieur interne : 000709 ( PascalFrancis/Checkpoint ); précédent : 000708; suivant : 000710Physiological 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.
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- Pascal (Inist)
English descriptors
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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.
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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. 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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>Brain derived neurotrophic factor</term><term>Corpus striatum</term><term>Glial cell line derived neurotrophic factor</term><term>Lesion</term><term>Melatonin</term><term>Models</term><term>Neuroprotection</term><term>Oxidopamine</term><term>Parkinson disease</term><term>Rat</term><term>Tyrosine 3-monooxygenase</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><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-8993</s0></fA01><fA02 i1="01"><s0>BRREAP</s0></fA02><fA03 i2="1"><s0>Brain res.</s0></fA03><fA05><s2>1068</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease</s1></fA08><fA11 i1="01" i2="1"><s1>SHARMA (Rohita)</s1></fA11><fA11 i1="02" i2="1"><s1>MCMILLAN (Catherine R.)</s1></fA11><fA11 i1="03" i2="1"><s1>TENN (Catherine C.)</s1></fA11><fA11 i1="04" i2="1"><s1>NILES (Lennard P.)</s1></fA11><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></fA14><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></fA14><fA20><s1>230-236</s1></fA20><fA21><s1>2006</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>12895</s2><s5>354000135326280260</s5></fA43><fA44><s0>0000</s0><s1>© 2006 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>30 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>06-0132091</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Brain research</s0></fA64><fA66 i1="01"><s0>NLD</s0></fA66><fC01 i1="01" l="ENG"><s0>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.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC02 i1="02" i2="X"><s0>002B17A01</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Neuroprotection</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Neuroprotection</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Neuroprotección</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Mélatonine</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Melatonin</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Melatonina</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Oxidopamine</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Oxidopamine</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Oxidopamina</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Modèle</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" 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(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)
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