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Active decorrelation in the basal ganglia.

C J Wilson1

  • 1Department of Biology, University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249, United States.

Neuroscience
|July 30, 2013
PubMed
Summary

Basal ganglia neurons are pacemaker cells that normally fire irregularly due to synaptic inputs. This irregular firing prevents synchronized activity, but its loss in Parkinson's disease may cause abnormal oscillations.

Keywords:
6-OHDA6-hydroxy dopamineEEGGPeGPiHCNParkinson’s diseaseSNrSTNelectroencephalographicexternal segments of the globus pallidushyperpolarization-activated cation currentinternal segments of the globus pallidusnetwork oscillationsphase-resettingspike-timingsubstantia nigra pars reticulatasubthalamic nucleussynchrony

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Area of Science:

  • Neuroscience
  • Computational Neuroscience
  • Systems Neuroscience

Background:

  • Basal ganglia nuclei (globus pallidus, subthalamic nucleus, substantia nigra) exhibit homogeneous cytoarchitecture, suggesting convergent inputs.
  • Local axon collaterals and inhibitory synapses within these nuclei hint at potential spike-time correlations among neurons.
  • Experimental studies have surprisingly failed to demonstrate these expected spike-time correlations.

Purpose of the Study:

  • To reconcile the expected spike-time correlations in basal ganglia circuitry with experimental findings.
  • To investigate the role of intrinsic neuronal properties, specifically pacemaking, in regulating spike timing.
  • To explore how basal ganglia connectivity and physiology might actively prevent synchronized neuronal activity.

Main Methods:

  • Analysis of firing patterns in basal ganglia cells, identifying them as pacemaker cells.
  • Theoretical and computational modeling of repetitively-firing neurons under shared inputs and synaptic coupling.
  • Examination of factors influencing spike-timing patterns, including pacemaking mechanisms, noise, firing rates, and synaptic properties.

Main Results:

  • Basal ganglia neurons function as pacemaker cells with intrinsically high firing rates, perturbed by synaptic noise.
  • Theoretical models demonstrate that neuronal pacemaking, noise, and synaptic properties critically shape spike-timing patterns.
  • The intrinsic properties and connectivity of the basal ganglia appear to be configured to actively decorrelate neuronal activity.

Conclusions:

  • The pacemaking nature of basal ganglia neurons, coupled with synaptic noise, explains the lack of observed spike-time correlations.
  • These mechanisms actively prevent permanent spike-timing relationships, maintaining functional independence of neuronal activity.
  • Loss of pacemaking and decorrelation mechanisms in Parkinson's disease may underlie the emergence of pathological synchronous oscillations.