MovDisordV3, PascalFrancis, Corpus, bibRecord, 000034

Thalamic Noradrenaline in Parkinson's Disease: Deficits Suggest Role in Motor and Non-Motor Symptoms

Identifieur interne : 000034 ( PascalFrancis/Corpus ); précédent : 000033; suivant : 000035

Thalamic Noradrenaline in Parkinson's Disease: Deficits Suggest Role in Motor and Non-Motor Symptoms

Auteurs : Christian Pifl ; Stephen J. Kish ; Oleh Hornykiewicz

Source :

Movement disorders [ 0885-3185 ] ; 2012.

RBID : Pascal:13-0017937

Descripteurs français

Pascal (Inist)
- Maladie de Parkinson, Trouble moteur, Pathologie du système nerveux.

English descriptors

KwdEn :
- Motor system disorder, Nervous system diseases, Parkinson disease.

Abstract

The thalamus occupies a pivotal position within the corticobasal ganglia-cortical circuits. In Parkinson's disease (PD), the thalamus exhibits pathological neuronal discharge patterns, foremost increased bursting and oscillatory activity, which are thought to perturb the faithful transfer of basal ganglia impulse flow to the cortex. Analogous abnormal thalamic discharge patterns develop in animals with experimentally reduced thalamic noradrenaline; conversely, added to thalamic neuronal preparations, noradrenaline exhibits marked anti-oscillatory and antibursting activity. Our study is based on this experimentally established link between noradrenaline and the quality of thalamic neuronal discharges. We analyzed 14 thalamic nuclei from all functionally relevant territories of 9 patients with PD and 8 controls, and measured noradrenaline with high-performance liquid chromatography with electrochemical detection. In PD, noradrenaline was profoundly reduced in all nuclei of the motor (pallidonigral and cerebellar) thalamus (ventroanterior: -86%, P = .0011; ventrolateral oral: -87%, P = .0010; ventrolateral caudal: -89%, P = .0014): Also, marked noradrenaline losses, ranging from 68% to 91% of controls, were found in other thalamic territories, including associative, limbic and intralaminar regions; the primary sensory regions were only mildly affected. The marked noradrenergic deafferentiation of the thalamus discloses a strategically located noradrenergic component in the overall pathophysiology of PD, suggesting a role in the complex mechanisms involved with the genesis of the motor and non-motor symptoms. Our study thus significantly contributes to the knowledge of the extrastriatal nondopaminergic mechanisms of PD with direct relevance to treatment of this disorder.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A03		`1`		`@0 Mov. disord.`
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A11	`01`	`1`		`@1 PIFL (Christian)`
A11	`02`	`1`		`@1 KISH (Stephen J.)`
A11	`03`	`1`		`@1 HORNYKIEWICZ (Oleh)`
A14	`01`			`@1 Center for Brain Research, Medical University of Vienna @2 Vienna @3 AUT @Z 1 aut. @Z 3 aut.`
A14	`02`			`@1 Human Brain Laboratory, Centre for Addiction and Mental Health @2 Toronto, Ontario @3 CAN @Z 2 aut.`
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A43	`01`			`@1 INIST @2 20953 @5 354000505459050110`
A44				`@0 0000 @1 © 2013 INIST-CNRS. All rights reserved.`
A45				`@0 59 ref.`
A47	`01`	`1`		`@0 13-0017937`
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A61				`@0 A`
A64	`01`	`1`		`@0 Movement disorders`
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C01	`01`		`ENG`	@0 The thalamus occupies a pivotal position within the corticobasal ganglia-cortical circuits. In Parkinson's disease (PD), the thalamus exhibits pathological neuronal discharge patterns, foremost increased bursting and oscillatory activity, which are thought to perturb the faithful transfer of basal ganglia impulse flow to the cortex. Analogous abnormal thalamic discharge patterns develop in animals with experimentally reduced thalamic noradrenaline; conversely, added to thalamic neuronal preparations, noradrenaline exhibits marked anti-oscillatory and antibursting activity. Our study is based on this experimentally established link between noradrenaline and the quality of thalamic neuronal discharges. We analyzed 14 thalamic nuclei from all functionally relevant territories of 9 patients with PD and 8 controls, and measured noradrenaline with high-performance liquid chromatography with electrochemical detection. In PD, noradrenaline was profoundly reduced in all nuclei of the motor (pallidonigral and cerebellar) thalamus (ventroanterior: -86%, P = .0011; ventrolateral oral: -87%, P = .0010; ventrolateral caudal: -89%, P = .0014): Also, marked noradrenaline losses, ranging from 68% to 91% of controls, were found in other thalamic territories, including associative, limbic and intralaminar regions; the primary sensory regions were only mildly affected. The marked noradrenergic deafferentiation of the thalamus discloses a strategically located noradrenergic component in the overall pathophysiology of PD, suggesting a role in the complex mechanisms involved with the genesis of the motor and non-motor symptoms. Our study thus significantly contributes to the knowledge of the extrastriatal nondopaminergic mechanisms of PD with direct relevance to treatment of this disorder.
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C07	`02`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 38`
C07	`02`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 38`
C07	`03`	`X`	`FRE`	`@0 Maladie dégénérative @5 39`
C07	`03`	`X`	`ENG`	`@0 Degenerative disease @5 39`
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C07	`04`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 40`
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C07	`04`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 40`
C07	`05`	`X`	`FRE`	`@0 Trouble neurologique @5 42`
C07	`05`	`X`	`ENG`	`@0 Neurological disorder @5 42`
C07	`05`	`X`	`SPA`	`@0 Trastorno neurológico @5 42`
N21				`@1 007`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 13-0017937 INIST
ET :	Thalamic Noradrenaline in Parkinson's Disease: Deficits Suggest Role in Motor and Non-Motor Symptoms
AU :	PIFL (Christian); KISH (Stephen J.); HORNYKIEWICZ (Oleh)
AF :	Center for Brain Research, Medical University of Vienna/Vienna/Autriche (1 aut., 3 aut.); Human Brain Laboratory, Centre for Addiction and Mental Health/Toronto, Ontario/Canada (2 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2012; Vol. 27; No. 13; Pp. 1618-1624; Bibl. 59 ref.
LA :	Anglais
EA :	The thalamus occupies a pivotal position within the corticobasal ganglia-cortical circuits. In Parkinson's disease (PD), the thalamus exhibits pathological neuronal discharge patterns, foremost increased bursting and oscillatory activity, which are thought to perturb the faithful transfer of basal ganglia impulse flow to the cortex. Analogous abnormal thalamic discharge patterns develop in animals with experimentally reduced thalamic noradrenaline; conversely, added to thalamic neuronal preparations, noradrenaline exhibits marked anti-oscillatory and antibursting activity. Our study is based on this experimentally established link between noradrenaline and the quality of thalamic neuronal discharges. We analyzed 14 thalamic nuclei from all functionally relevant territories of 9 patients with PD and 8 controls, and measured noradrenaline with high-performance liquid chromatography with electrochemical detection. In PD, noradrenaline was profoundly reduced in all nuclei of the motor (pallidonigral and cerebellar) thalamus (ventroanterior: -86%, P = .0011; ventrolateral oral: -87%, P = .0010; ventrolateral caudal: -89%, P = .0014): Also, marked noradrenaline losses, ranging from 68% to 91% of controls, were found in other thalamic territories, including associative, limbic and intralaminar regions; the primary sensory regions were only mildly affected. The marked noradrenergic deafferentiation of the thalamus discloses a strategically located noradrenergic component in the overall pathophysiology of PD, suggesting a role in the complex mechanisms involved with the genesis of the motor and non-motor symptoms. Our study thus significantly contributes to the knowledge of the extrastriatal nondopaminergic mechanisms of PD with direct relevance to treatment of this disorder.
CC :	002B17; 002B17G
FD :	Maladie de Parkinson; Trouble moteur; Pathologie du système nerveux
FG :	Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Trouble neurologique
ED :	Parkinson disease; Motor system disorder; Nervous system diseases
EG :	Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Neurological disorder
SD :	Parkinson enfermedad; Trastorno motor; Sistema nervioso patología
LO :	INIST-20953.354000505459050110
ID :	13-0017937

Links to Exploration step

Pascal:13-0017937

Le document en format XML

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<front><div type="abstract" xml:lang="en">The thalamus occupies a pivotal position within the corticobasal ganglia-cortical circuits. In Parkinson's disease (PD), the thalamus exhibits pathological neuronal discharge patterns, foremost increased bursting and oscillatory activity, which are thought to perturb the faithful transfer of basal ganglia impulse flow to the cortex. Analogous abnormal thalamic discharge patterns develop in animals with experimentally reduced thalamic noradrenaline; conversely, added to thalamic neuronal preparations, noradrenaline exhibits marked anti-oscillatory and antibursting activity. Our study is based on this experimentally established link between noradrenaline and the quality of thalamic neuronal discharges. We analyzed 14 thalamic nuclei from all functionally relevant territories of 9 patients with PD and 8 controls, and measured noradrenaline with high-performance liquid chromatography with electrochemical detection. In PD, noradrenaline was profoundly reduced in all nuclei of the motor (pallidonigral and cerebellar) thalamus (ventroanterior: -86%, P = .0011; ventrolateral oral: -87%, P = .0010; ventrolateral caudal: -89%, P = .0014): Also, marked noradrenaline losses, ranging from 68% to 91% of controls, were found in other thalamic territories, including associative, limbic and intralaminar regions; the primary sensory regions were only mildly affected. The marked noradrenergic deafferentiation of the thalamus discloses a strategically located noradrenergic component in the overall pathophysiology of PD, suggesting a role in the complex mechanisms involved with the genesis of the motor and non-motor symptoms. Our study thus significantly contributes to the knowledge of the extrastriatal nondopaminergic mechanisms of PD with direct relevance to treatment of this disorder.</div>
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<ET>Thalamic Noradrenaline in Parkinson's Disease: Deficits Suggest Role in Motor and Non-Motor Symptoms</ET>
<AU>PIFL (Christian); KISH (Stephen J.); HORNYKIEWICZ (Oleh)</AU>
<AF>Center for Brain Research, Medical University of Vienna/Vienna/Autriche (1 aut., 3 aut.); Human Brain Laboratory, Centre for Addiction and Mental Health/Toronto, Ontario/Canada (2 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2012; Vol. 27; No. 13; Pp. 1618-1624; Bibl. 59 ref.</SO>
<LA>Anglais</LA>
<EA>The thalamus occupies a pivotal position within the corticobasal ganglia-cortical circuits. In Parkinson's disease (PD), the thalamus exhibits pathological neuronal discharge patterns, foremost increased bursting and oscillatory activity, which are thought to perturb the faithful transfer of basal ganglia impulse flow to the cortex. Analogous abnormal thalamic discharge patterns develop in animals with experimentally reduced thalamic noradrenaline; conversely, added to thalamic neuronal preparations, noradrenaline exhibits marked anti-oscillatory and antibursting activity. Our study is based on this experimentally established link between noradrenaline and the quality of thalamic neuronal discharges. We analyzed 14 thalamic nuclei from all functionally relevant territories of 9 patients with PD and 8 controls, and measured noradrenaline with high-performance liquid chromatography with electrochemical detection. In PD, noradrenaline was profoundly reduced in all nuclei of the motor (pallidonigral and cerebellar) thalamus (ventroanterior: -86%, P = .0011; ventrolateral oral: -87%, P = .0010; ventrolateral caudal: -89%, P = .0014): Also, marked noradrenaline losses, ranging from 68% to 91% of controls, were found in other thalamic territories, including associative, limbic and intralaminar regions; the primary sensory regions were only mildly affected. The marked noradrenergic deafferentiation of the thalamus discloses a strategically located noradrenergic component in the overall pathophysiology of PD, suggesting a role in the complex mechanisms involved with the genesis of the motor and non-motor symptoms. Our study thus significantly contributes to the knowledge of the extrastriatal nondopaminergic mechanisms of PD with direct relevance to treatment of this disorder.</EA>
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<FG>Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du   système nerveux central; Trouble neurologique</FG>
<ED>Parkinson disease; Motor system disorder; Nervous system diseases</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Neurological disorder</EG>
<SD>Parkinson enfermedad; Trastorno motor; Sistema nervioso patología</SD>
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<ID>13-0017937</ID>
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	Movement Disorders (revue)
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Movement Disorders (revue)

Thalamic Noradrenaline in Parkinson's Disease: Deficits Suggest Role in Motor and Non-Motor Symptoms

Thalamic Noradrenaline in Parkinson's Disease: Deficits Suggest Role in Motor and Non-Motor Symptoms

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