The Experts below are selected from a list of 624 Experts worldwide ranked by ideXlab platform

Miguel a L. Nicolelis - One of the best experts on this subject based on the ideXlab platform.

  • rapid alterations in corticostriatal ensemble coordination during acute dopamine dependent motor dysfunction
    Neuron, 2006
    Co-Authors: Raul r Gainetdinov, Rui M Costa, Shih-chieh Lin, Tatyana D Sotnikova, Michel Cyr, Marc G Caron, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia ( approximately 500% of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons ( approximately 70%) changed firing rate during the transition between dopamine-related Hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During Hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson's disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits.

  • Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction
    Neuron, 2006
    Co-Authors: Rui M Costa, Tatyana d Sotnikova, Raul r Gainetdinov, Marc g Caron, Michael Cyr, Shih-chieh Lin, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (∼500% of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (

  • Rapid alterations in corticostriatal ensemble coordination during acute dopamine-dependent motor dysfunction
    2006
    Co-Authors: Rui M Costa, Raul r Gainetdinov, Shih-chieh Lin, Tatyana D Sotnikova, Michel Cyr, Marc G Caron, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopaminerelated motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (w500 % of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons (w70%) changed firing rate during the transition between dopamine-related Hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During Hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson’s disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits

Rui M Costa - One of the best experts on this subject based on the ideXlab platform.

  • rapid alterations in corticostriatal ensemble coordination during acute dopamine dependent motor dysfunction
    Neuron, 2006
    Co-Authors: Raul r Gainetdinov, Rui M Costa, Shih-chieh Lin, Tatyana D Sotnikova, Michel Cyr, Marc G Caron, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia ( approximately 500% of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons ( approximately 70%) changed firing rate during the transition between dopamine-related Hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During Hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson's disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits.

  • Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction
    Neuron, 2006
    Co-Authors: Rui M Costa, Tatyana d Sotnikova, Raul r Gainetdinov, Marc g Caron, Michael Cyr, Shih-chieh Lin, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (∼500% of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (

  • Rapid alterations in corticostriatal ensemble coordination during acute dopamine-dependent motor dysfunction
    2006
    Co-Authors: Rui M Costa, Raul r Gainetdinov, Shih-chieh Lin, Tatyana D Sotnikova, Michel Cyr, Marc G Caron, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopaminerelated motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (w500 % of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons (w70%) changed firing rate during the transition between dopamine-related Hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During Hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson’s disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits

Christos Ganos - One of the best experts on this subject based on the ideXlab platform.

  • Teaching Video NeuroImages: Paroxysmal Hyperkinesia with diurnal fluctuations due to sepiapterin-reductase deficiency.
    Neurology, 2020
    Co-Authors: Tina Mainka, Jessica Hoffmann, Andrea A. Kühn, Saskia Biskup, Christos Ganos
    Abstract:

    A 42-year-old man, born of consanguineous parents, presented with long-standing severe, nonepileptic jerky movements of the upper body, pronounced during the second half of the day and improving after sleep (video, A and B). There was a history of neurodevelopmental disorder with axial hypotonia, delayed milestones, intellectual disability, and poor speech production. The combination of a neurodevelopmental syndrome and a movement disorder with diurnal fluctuations1 led to targeted exome sequencing for monoamine metabolism disorders. A homozygous nonsense variant in the SPR gene was identified (figure), confirmed by Sanger sequencing (figure). Treatment with levodopa led to marked improvement of abnormal movements (video, C).

  • paroxysmal kinesigenic dyskinesia may be misdiagnosed in co occurring gilles de la tourette syndrome
    Movement Disorders Clinical Practice, 2014
    Co-Authors: Roberto Erro, Christos Ganos, Niccolo E Mencacci, A Gardiner, Amit Batla, Henry Houlden
    Abstract:

    Tics, particularly at a young age, may be difficult to distinguish from other abrupt and brief movements, such as myoclonus and chorea. Their suppressibility and association with premonitory urges serve as useful diagnostic clues. However, not all individuals with tics or Gilles de la Tourette syndrome (GTS) are able to exert conscious inhibitory tic control and not all tics are preceded by premonitory sensations. Furthermore, Hyperkinesias in other paroxysmal movement disorders, such as in paroxysmal kinesigenic dyskinesia (PKD), a condition associated with several episodic neurologic disorders and for which a causative gene has been recently described,1 are commonly preceded by sensory phenomena, such as numbness of the affected body sites or epigastric area.1–3 Moreover, the presence of dystonic tics, which differ from clonic tics in phenomenology and duration, might further contribute to diagnostic confusion.4–7 On the other hand, not all sudden and repetitive movements in GTS are tics and more than one Hyperkinesia may co-occur in a single patient. Their proper recognition bears significant prognostic and therapeutic implications. Here, we present the case of an adolescent with a classic history of GTS, who was referred to our clinic upon developing longer-lasting and, on occasion, disabling hyperkinetic episodes at a later age misdiagnosed as complex tics.

Shih-chieh Lin - One of the best experts on this subject based on the ideXlab platform.

  • rapid alterations in corticostriatal ensemble coordination during acute dopamine dependent motor dysfunction
    Neuron, 2006
    Co-Authors: Raul r Gainetdinov, Rui M Costa, Shih-chieh Lin, Tatyana D Sotnikova, Michel Cyr, Marc G Caron, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia ( approximately 500% of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons ( approximately 70%) changed firing rate during the transition between dopamine-related Hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During Hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson's disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits.

  • Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction
    Neuron, 2006
    Co-Authors: Rui M Costa, Tatyana d Sotnikova, Raul r Gainetdinov, Marc g Caron, Michael Cyr, Shih-chieh Lin, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (∼500% of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (

  • Rapid alterations in corticostriatal ensemble coordination during acute dopamine-dependent motor dysfunction
    2006
    Co-Authors: Rui M Costa, Raul r Gainetdinov, Shih-chieh Lin, Tatyana D Sotnikova, Michel Cyr, Marc G Caron, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopaminerelated motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (w500 % of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons (w70%) changed firing rate during the transition between dopamine-related Hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During Hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson’s disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits

Raul r Gainetdinov - One of the best experts on this subject based on the ideXlab platform.

  • rapid alterations in corticostriatal ensemble coordination during acute dopamine dependent motor dysfunction
    Neuron, 2006
    Co-Authors: Raul r Gainetdinov, Rui M Costa, Shih-chieh Lin, Tatyana D Sotnikova, Michel Cyr, Marc G Caron, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia ( approximately 500% of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons ( approximately 70%) changed firing rate during the transition between dopamine-related Hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During Hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson's disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits.

  • Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction
    Neuron, 2006
    Co-Authors: Rui M Costa, Tatyana d Sotnikova, Raul r Gainetdinov, Marc g Caron, Michael Cyr, Shih-chieh Lin, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (∼500% of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (

  • Rapid alterations in corticostriatal ensemble coordination during acute dopamine-dependent motor dysfunction
    2006
    Co-Authors: Rui M Costa, Raul r Gainetdinov, Shih-chieh Lin, Tatyana D Sotnikova, Michel Cyr, Marc G Caron, Miguel a L. Nicolelis
    Abstract:

    Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopaminerelated motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (w500 % of controls) with Hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons (w70%) changed firing rate during the transition between dopamine-related Hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During Hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson’s disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits