Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Cellular principles underlying normal and pathological activity in the subthalamic nucleus.

Mark D Bevan1, Jeremy F Atherton, Jérôme Baufreton

  • 1Northwestern University, Department of Physiology, Feinberg School of Medicine, 303 East Chicago Avenue, Chicago, IL 60611, USA. m-bevan@northwestern.edu

Current Opinion in Neurobiology
|November 7, 2006
PubMed
Summary

Parkinson's disease motor symptoms stem from abnormal brain activity. Dopamine loss disrupts signals in the basal ganglia, causing pathological rhythms that worsen motor control.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Locus coeruleus α-synuclein overexpression induces prodromal Parkinsonian features in mice.

NPJ Parkinson's disease·2026
Same author

Dorsal Raphe VIP Neurons Are Critical for Survival-Oriented Vigilance.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Movement-related increases in subthalamic activity optimize locomotion.

Cell reports·2025
Same author

Developmental alterations of indirect-pathway medium spiny neurons in mouse models of Huntington's disease.

Neurobiology of disease·2025
Same author

GAP43 Located on Corticostriatal Terminals Restrains Novelty-Induced Hyperactivity in Mice.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2024
Same author

A population of Insula neurons encodes for social preference only after acute social isolation in mice.

Nature communications·2024

Area of Science:

  • Neuroscience
  • Movement Disorders
  • Basal Ganglia Function

Background:

  • Motor symptoms in Parkinson's disease (PD) correlate with abnormal, rhythmic, low-frequency activity in the subthalamic nucleus (STN) and connected basal ganglia nuclei.
  • Therapies targeting STN activity, like deep brain stimulation (DBS) and levodopa, offer symptomatic relief for PD motor deficits.
  • Understanding the mechanisms governing STN activity is crucial for developing more effective PD treatments.

Purpose of the Study:

  • To investigate how dopamine denervation in Parkinson's disease alters neuronal signaling within the basal ganglia.
  • To elucidate the mechanisms by which altered synaptic inputs lead to pathological network activity in the STN.
  • To connect these circuit-level changes to the emergence of motor symptoms in Parkinson's disease.

Related Experiment Videos

Main Methods:

  • Analysis of synaptic transmission and integration of cortical and pallidal inputs to STN neurons in models of dopamine denervation.
  • Electrophysiological recordings to characterize neuronal activity patterns in the STN and related basal ganglia structures.
  • Investigating the role of glutamatergic and GABAergic pathways in the pathophysiology of Parkinson's disease.

Main Results:

  • Dopamine denervation profoundly disrupts the normal transmission and integration of excitatory (glutamatergic) and inhibitory (GABAergic) inputs to STN neurons.
  • This disruption leads to abnormal, pathological network activity characterized by low-frequency, rhythmic bursting.
  • The pathological activity resonates throughout the basal ganglia and the broader motor system, correlating with motor deficits.

Conclusions:

  • Dopamine loss in Parkinson's disease fundamentally alters basal ganglia circuit function by impairing synaptic input processing in the STN.
  • These alterations generate pathological network oscillations that are a key mechanism underlying motor symptoms.
  • Targeting these aberrant signaling pathways offers a potential strategy for novel Parkinson's disease therapies.