ParkinsonCanadaV1, PascalFrancis, Curation, bibRecord, 000453

MPTP induces intranuclear rodlet formation in midbrain dopaminergic neurons

Identifieur interne : 000453 ( PascalFrancis/Curation ); précédent : 000452; suivant : 000454

MPTP induces intranuclear rodlet formation in midbrain dopaminergic neurons

Auteurs : Wiplove Lamba [Canada] ; Wendy Prichett [Canada] ; David Munoz [Canada] ; David S. Park [Canada] ; John M. Woulfe [Canada]

Source :

Brain research [ 0006-8993 ] ; 2005.

RBID : Pascal:06-0062122

Descripteurs français

Pascal (Inist)
- Neurotoxine, Mésencéphale, Neurone dopaminergique, Tubuline, Parkinson maladie, Souris, Animal, MPTP.

English descriptors

KwdEn :
- Animal, Dopaminergic neuron, Midbrain, Mouse, Neurotoxin, Parkinson disease, Tubulin.

Abstract

Neuronal intranuclear rodlets (INRs; rodlets of Roncoroni) have been known to neuroanatomists since the turn of the century. However, the functional and/or pathological significance of these structures has remained enigmatic. We recently demonstrated that these structures are immunoreactive for class III β tubulin and for glucocorticoid receptor. Moreover, they are markedly reduced in the temporal cortex of patients with Alzheimer's disease relative to age-matched controls and those with dementia with Lewy bodies, thereby implicating these structures in neurodegenerative disease pathogenesis. The present report represents an experimental pilot study to investigate the possible involvement of INRs in Parkinson's disease (PD). Specifically, we demonstrate significantly increased INRs in dopaminergic neurons in the substantia nigra pars compacta and ventral tegmental area in mice treated with the selective catecholaminergic neurotoxin MPTP, relative to saline-treated controls. We have hypothesized that INRs represent an intranuclear sequestrum of monomeric β-tubulin and that their alteration in neurodegeneration may reflect disrupted or abnormal microtubule dynamics. We propose that the increased formation of INRs is related to the demonstrated ability of MPTP to cause microtubule disruption. Because tubulin has also been implicated in the pathogenesis of human PD, it is possible that the results of this study will have important implications for this most common neurodegenerative movement disorder.

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A11	`02`	`1`		`@1 PRICHETT (Wendy)`
A11	`03`	`1`		`@1 MUNOZ (David)`
A11	`04`	`1`		`@1 PARK (David S.)`
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C01	`01`		`ENG`	@0 Neuronal intranuclear rodlets (INRs; rodlets of Roncoroni) have been known to neuroanatomists since the turn of the century. However, the functional and/or pathological significance of these structures has remained enigmatic. We recently demonstrated that these structures are immunoreactive for class III β tubulin and for glucocorticoid receptor. Moreover, they are markedly reduced in the temporal cortex of patients with Alzheimer's disease relative to age-matched controls and those with dementia with Lewy bodies, thereby implicating these structures in neurodegenerative disease pathogenesis. The present report represents an experimental pilot study to investigate the possible involvement of INRs in Parkinson's disease (PD). Specifically, we demonstrate significantly increased INRs in dopaminergic neurons in the substantia nigra pars compacta and ventral tegmental area in mice treated with the selective catecholaminergic neurotoxin MPTP, relative to saline-treated controls. We have hypothesized that INRs represent an intranuclear sequestrum of monomeric β-tubulin and that their alteration in neurodegeneration may reflect disrupted or abnormal microtubule dynamics. We propose that the increased formation of INRs is related to the demonstrated ability of MPTP to cause microtubule disruption. Because tubulin has also been implicated in the pathogenesis of human PD, it is possible that the results of this study will have important implications for this most common neurodegenerative movement disorder.
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Pascal:06-0062122

Le document en format XML

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<front><div type="abstract" xml:lang="en">Neuronal intranuclear rodlets (INRs; rodlets of Roncoroni) have been known to neuroanatomists since the turn of the century. However, the functional and/or pathological significance of these structures has remained enigmatic. We recently demonstrated that these structures are immunoreactive for class III β tubulin and for glucocorticoid receptor. Moreover, they are markedly reduced in the temporal cortex of patients with Alzheimer's disease relative to age-matched controls and those with dementia with Lewy bodies, thereby implicating these structures in neurodegenerative disease pathogenesis. The present report represents an experimental pilot study to investigate the possible involvement of INRs in Parkinson's disease (PD). Specifically, we demonstrate significantly increased INRs in dopaminergic neurons in the substantia nigra pars compacta and ventral tegmental area in mice treated with the selective catecholaminergic neurotoxin MPTP, relative to saline-treated controls. We have hypothesized that INRs represent an intranuclear sequestrum of monomeric β-tubulin and that their alteration in neurodegeneration may reflect disrupted or abnormal microtubule dynamics. We propose that the increased formation of INRs is related to the demonstrated ability of MPTP to cause microtubule disruption. Because tubulin has also been implicated in the pathogenesis of human PD, it is possible that the results of this study will have important implications for this most common neurodegenerative movement disorder.</div>
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<fC01 i1="01" l="ENG"><s0>Neuronal intranuclear rodlets (INRs; rodlets of Roncoroni) have been known to neuroanatomists since the turn of the century. However, the functional and/or pathological significance of these structures has remained enigmatic. We recently demonstrated that these structures are immunoreactive for class III β tubulin and for glucocorticoid receptor. Moreover, they are markedly reduced in the temporal cortex of patients with Alzheimer's disease relative to age-matched controls and those with dementia with Lewy bodies, thereby implicating these structures in neurodegenerative disease pathogenesis. The present report represents an experimental pilot study to investigate the possible involvement of INRs in Parkinson's disease (PD). Specifically, we demonstrate significantly increased INRs in dopaminergic neurons in the substantia nigra pars compacta and ventral tegmental area in mice treated with the selective catecholaminergic neurotoxin MPTP, relative to saline-treated controls. We have hypothesized that INRs represent an intranuclear sequestrum of monomeric β-tubulin and that their alteration in neurodegeneration may reflect disrupted or abnormal microtubule dynamics. We propose that the increased formation of INRs is related to the demonstrated ability of MPTP to cause microtubule disruption. Because tubulin has also been implicated in the pathogenesis of human PD, it is possible that the results of this study will have important implications for this most common neurodegenerative movement disorder.</s0>
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<fC03 i1="03" i2="X" l="ENG"><s0>Dopaminergic neuron</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Neurona dopaminérgica</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Tubuline</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Tubulin</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Tubulina</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>09</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Souris</s0>
<s5>54</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Mouse</s0>
<s5>54</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Ratón</s0>
<s5>54</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Animal</s0>
<s5>69</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Animal</s0>
<s5>69</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Animal</s0>
<s5>69</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>MPTP</s0>
<s4>INC</s4>
<s5>78</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Toxine</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Toxin</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Toxina</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>20</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>21</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>22</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>23</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>24</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>25</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>037</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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   |texte=   MPTP induces intranuclear rodlet formation in midbrain dopaminergic neurons
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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)
	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)

MPTP induces intranuclear rodlet formation in midbrain dopaminergic neurons

MPTP induces intranuclear rodlet formation in midbrain dopaminergic neurons

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Abstract

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