Thalamic Noradrenaline in Parkinson's Disease: Deficits Suggest Role in Motor and Non-Motor Symptoms
Identifieur interne : 000F65 ( Main/Curation ); précédent : 000F64; suivant : 000F66Thalamic Noradrenaline in Parkinson's Disease: Deficits Suggest Role in Motor and Non-Motor Symptoms
Auteurs : Christian Pifl [Autriche] ; Stephen J. Kish [Canada] ; Oleh Hornykiewicz [Autriche]Source :
- Movement disorders [ 0885-3185 ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- MESH :
- chemical , deficiency : Norepinephrine.
- metabolism : Parkinson Disease, Thalamus.
- pathology : Neurons, Parkinson Disease, Thalamus.
- Aged, Aged, 80 and over, Cell Death, Female, Humans, Male.
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.
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Pascal:13-0017937Le 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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<idno type="ISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<imprint><date when="2012">2012</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term>
<term>Aged, 80 and over</term>
<term>Cell Death</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Neurons (pathology)</term>
<term>Norepinephrine (deficiency)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Parkinson Disease (pathology)</term>
<term>Thalamus (metabolism)</term>
<term>Thalamus (pathology)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Norepinephrine</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term>
<term>Thalamus</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurons</term>
<term>Parkinson Disease</term>
<term>Thalamus</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Aged, 80 and over</term>
<term>Cell Death</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title>
<p id="P1">The thalamus occupies a pivotal position within the cortico-basal ganglia-cortical circuits. In Parkinson's disease, 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 anti-bursting activity. Our study is based on this experimentally established link between noradrenaline and the quality of thalamic neuronal discharges.</p>
</sec>
<sec id="S2"><title>Methods</title>
<p id="P2">We analysed fourteen thalamic nuclei from all functionally relevant territories of nine patients with Parkinson's disease and eight controls and measured noradrenaline with high pressure liquid chromatography with electrochemical detection.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">In Parkinson's disease, noradrenaline was profoundly reduced in all nuclei of the motor (pallidonigral and cerebellar) thalamus (ventroanterior: -86%, p=0.0011; ventrolateral oral: -87%, p=0.0010; ventrolateral caudal: -89%, p=0.0014): 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.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">The marked noradrenergic deafferentiation of the thalamus discloses a strategically located noradrenergic component in the overall pathophysiology of the Parkinson's disease, 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 non-dopaminergic mechanisms of Parkinson's disease with direct relevance to treatment of this disorder.</p>
</sec>
</div>
</front>
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