ParkinsonCanadaV1, PascalFrancis, Curation, bibRecord, 000463

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

Identifieur interne : 000463 ( PascalFrancis/Curation ); précédent : 000462; suivant : 000464

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, Brain derived neurotrophic factor, Corpus striatum, Glial cell line derived neurotrophic factor, Lesion, Melatonin, Models, Neuroprotection, Oxidopamine, Parkinson disease, Rat, Tyrosine 3-monooxygenase.

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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<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>
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<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>
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<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" l="ENG"><s0>Models</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Modelo</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Lésion</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Lesion</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Lesión</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Corps strié</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Corpus striatum</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Cuerpo estriado</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Tyrosine 3-monooxygenase</s0>
<s2>FE</s2>
<s5>07</s5>
<s6>Tyrosine «3»-monooxygenase</s6>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Tyrosine 3-monooxygenase</s0>
<s2>FE</s2>
<s5>07</s5>
<s6>Tyrosine «3»-monooxygenase</s6>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Tyrosine 3-monooxygenase</s0>
<s2>FE</s2>
<s5>07</s5>
<s6>Tyrosine «3»-monooxygenase</s6>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Facteur GDNF</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Glial cell line derived neurotrophic factor</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Factor GDNF</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Facteur BDNF</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Brain derived neurotrophic factor</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Factor BDNF</s0>
<s5>10</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Rat</s0>
<s5>54</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Rat</s0>
<s5>54</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Rata</s0>
<s5>54</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Animal</s0>
<s5>69</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Animal</s0>
<s5>69</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Animal</s0>
<s5>69</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Hormone épiphysaire</s0>
<s5>20</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Pineal hormone</s0>
<s5>20</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Hormona epifisaria</s0>
<s5>20</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>21</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>21</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>21</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>22</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>22</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>22</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>23</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>23</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>23</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>24</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>24</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>24</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>25</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>25</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>25</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Noyau gris central</s0>
<s5>26</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Basal ganglion</s0>
<s5>26</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Núcleo basal</s0>
<s5>26</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>27</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>27</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>27</s5>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="12" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="12" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="12" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="13" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="13" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="13" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>079</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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   |texte=   Physiological neuroprotection by melatonin in a 6-hydroxydopamine model of Parkinson's disease
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	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.

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

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