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Updated: Mar 17, 2026

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Corticostriatal Dysfunction in Huntington's Disease: The Basics.

Kendra D Bunner1, George V Rebec1

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|July 23, 2016
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Summary

Huntington's disease (HD) involves early corticostriatal pathway damage. Glutamate and dopamine dysregulation contribute to HD symptoms, highlighting targets for future Huntington's disease therapeutics.

Keywords:
Huntington’s diseasecortiostriatal circuitrydopamineelectrophysiologyglutamate

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Area of Science:

  • Neuroscience
  • Neurodegenerative Diseases
  • Molecular Biology

Background:

  • Huntington's disease (HD) is an inherited neurodegenerative disorder characterized by progressive cognitive, emotional, and motor decline.
  • The corticostriatal pathway, a primary input to the basal ganglia, exhibits early neuropathological changes in HD.
  • Current treatments for HD are limited, necessitating further research into disease mechanisms.

Purpose of the Study:

  • To investigate the role of glutamate (Glu) and dopamine (DA) dysregulation in the corticostriatal pathway in the context of Huntington's disease.
  • To understand how altered neurotransmission contributes to the loss of information flow and the HD behavioral phenotype.
  • To identify potential therapeutic targets for HD by analyzing neurochemical and neurobehavioral changes.

Main Methods:

  • Utilizing transgenic animal models of Huntington's disease.
  • Analyzing corticostriatal glutamate (Glu) transmission, including postsynaptic receptors and Glu transport proteins.
  • Investigating the modulatory role of dopamine (DA) in Glu activation within the basal ganglia.
  • Conducting neurobehavioral analyses in HD models.

Main Results:

  • Early neuropathology in HD affects the corticostriatal pathway, impacting basal ganglia function.
  • Dysregulation of glutamate (Glu) transmission is implicated in the onset and progression of HD.
  • Altered dopamine (DA) signaling further exacerbates deficits in neuronal communication.
  • These neurochemical changes correlate with the development of the HD behavioral phenotype.

Conclusions:

  • Aberrant glutamate (Glu) and dopamine (DA) neurotransmission are critical factors in Huntington's disease (HD) pathogenesis.
  • Understanding corticostriatal Glu transmission and DA modulation is crucial for developing effective HD therapeutics.
  • Targeting these neurochemical pathways in the basal ganglia may offer a promising strategy for HD treatment.