Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Alterations in Muscle Tone ll

Alterations in Muscle Tone ll

Alterations in muscle tone are common manifestations of neurological disorders and reflect dysfunction within different nervous system regions. Spasticity, paratonia, and dystonia represent distinct forms of hypertonia, each with unique mechanisms, clinical features, and diagnostic importance.CharacteristicsSpasticity happens from upper motor neuron lesions and is characterized by velocity-dependent resistance to passive movement. Clinical features include:Exaggerated deep tendon reflexesClonus...

Parkinson's Disease: Treatment

Parkinson's Disease: Treatment

Neurodegenerative disorders, such as Parkinson's Disease (PD), involve the gradual and irreversible destruction of neurons in particular brain areas. These disorders exhibit standard features like proteinopathies, selective vulnerability of some neurons, and an interaction of intrinsic properties, genetics, and environmental influences in neural injury.
Parkinson's Disease is primarily a result of the loss of dopaminergic neurons in the substantia nigra pars compacta. The cornerstone of its...

Alterations in Muscle Tone lll

Alterations in Muscle Tone lll

Rigidity and myotonia are distinct abnormalities of muscle tone that affect resistance and relaxation during movement. Although both involve altered muscle contraction, they arise from different neurological and muscular mechanisms.CharacteristicsRigidity is characterized by uniform resistance to passive movement across the entire range, independent of speed, affecting flexors and extensors equally. It may appear as lead-pipe rigidity (smooth, constant resistance) or cogwheel rigidity...

Parkinson Disease ll: Pathophysiology

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...

Parkinson's Disease: Overview

Parkinson's Disease: Overview

Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is to...

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

Directly acting muscle relaxants like dantrolene and botulinum toxin (BoNT) have distinct mechanisms and applications. Dantrolene, a hydantoin derivative, acts on the ryanodine receptor (RYR1) in skeletal muscle cells. RYR1 are calcium channels present at the sarcoplasmic reticulum membrane. In response to excitation, they release calcium ions from the sarcoplasmic reticulum to the cytosol. Calcium promotes actin-myosin-mediated contraction of muscles.
The binding of dantrolene to the RYR1...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Spontaneous tauopathy with parkinsonism in an aged cynomolgus macaque.

Frontiers in aging neuroscience·2026

Same author

Lentiviral Vector Administration into the Mouse Brain.

Methods in molecular biology (Clifton, N.J.)·2025

Same author

Distinct roles of two thalamostriatal systems in visually triggered decision-making in common marmosets.

iScience·2025

Same author

Distinct brain network structure of mesial temporal lobe epilepsy compared to that of neocortical epilepsy: functional MRI study with surgically treated patients.

Journal of neurosurgery·2024

Same author

Sensory-motor circuit is a therapeutic target for <i>dystonia musculorum</i> mice, a model of hereditary sensory and autonomic neuropathy 6.

Science advances·2024

Same author

[Dynamic activity model of movement disorders: a unified view to understand their pathophysiology].

Rinsho shinkeigaku = Clinical neurology·2024

Search research articles

Related Experiment Video

Updated: May 26, 2026

Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia

Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia

Published on: September 12, 2020

Reduced pallidal output causes dystonia.

Atsushi Nambu¹, Satomi Chiken, Pullanipally Shashidharan

¹Division of System Neurophysiology, National Institute for Physiological Sciences and Department of Physiological Sciences, Graduate University for Advanced Studies Okazaki, Japan.

Frontiers in Systems Neuroscience

|December 14, 2011

Summary

Electrophysiological studies reveal abnormal globus pallidus activity in dystonia models and patients. Reduced output from the globus pallidus internal segment (GPi) may drive the involuntary movements characteristic of this neurological disorder.

Keywords:

dystonia extracellular recording globus pallidus movement disorders stereotactic surgery

More Related Videos

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Published on: October 4, 2021

MALDI Imaging Mass Spectrometry of Neuropeptides in Parkinson's Disease

MALDI Imaging Mass Spectrometry of Neuropeptides in Parkinson's Disease

Published on: February 14, 2012

Related Experiment Videos

Last Updated: May 26, 2026

Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia

Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia

Published on: September 12, 2020

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease

Published on: October 4, 2021

MALDI Imaging Mass Spectrometry of Neuropeptides in Parkinson's Disease

MALDI Imaging Mass Spectrometry of Neuropeptides in Parkinson's Disease

Published on: February 14, 2012

Area of Science:

Neuroscience
Neurology
Movement Disorders

Background:

Dystonia is a neurological disorder causing involuntary muscle contractions and abnormal postures.
Understanding the pathophysiology of dystonia is crucial for developing effective treatments.

Purpose of the Study:

To investigate the electrophysiological characteristics of dystonia using transgenic mouse models and a human patient.
To elucidate the role of the globus pallidus in dystonia pathophysiology.

Main Methods:

Electrophysiological recordings in awake DYT1 dystonia model mice.
Electrical stimulation of the primary motor cortex in mice and a human cervical dystonia patient.
Analysis of neuronal activity in the globus pallidus (GPi and GPe).

Main Results:

DYT1 dystonia model mice showed reduced spontaneous activity in the globus pallidus with abnormal bursts and pauses.
Motor cortex stimulation evoked long-lasting inhibition in the globus pallidus of dystonia models and patients, unlike in normal mice.
Somatotopic organization was disrupted in the globus pallidus of dystonia model mice.

Conclusions:

Reduced output from the globus pallidus internal segment (GPi) is a potential key mechanism in dystonia.
This reduced GPi output may lead to increased thalamic and cortical activity, causing dystonic movements.