Excitatory amino acid binding sites in the caudate nucleus and frontal cortex of huntington's disease

Academic Article


  • Huntington's disease is a dominantly inherited, progressive neurodegenerative disorder causing marked pathology in the basal ganglia. The pathophysiology of the selective neuronal death in as yet unknown, but evidence suggests that the neurotoxicity may result from endogenous substances acting at excitatory amino acid receptors. Previous data have shown a selective decrease in binding to one class of glutamate receptors, the N‐methyl‐D‐aspartate (NMDA) receptor in the putamen of Huntington's disease. The present study was undertaken to determine the relative density of binding to all of the currently defined subpopulations of excitatory amino acid receptors in the caudate nuclei and frontal cortex of patients with Huntington's disease and of control subjects, using quantitative in vitro autoradiography. NMDA, MK‐801, glycine, kainate, and α‐amino‐3‐hydroxy‐5‐methylisoxazole propionic acid (AMPA) receptor binding were all decreased to a similar extent (50–60°). Binding to the metabotropic quisqualate receptor and to the non‐NMDA, nonkainate, nonquisqualate (NNKQ) site was decreased nonsignificantly by 31° and 26°, respectively. Autoradiograms of NMDA, MK‐801, AMPA, kainate, metabotropic, and NNKQ receptors in caudates revealed an inhomogeneous pattern of binding that is different from the binding pattern seen in control caudates. Binding to all receptor subtypes was the same in the frontal cortex from Huntington's disease patients and control subjects. The data suggest that no single excitatory amino acid receptor is selectively decreased in the caudate of Huntington's disease. Copyright © 1991 American Neurological Association
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    Digital Object Identifier (doi)

    Author List

  • Dure LS; Young AB; Penney JB
  • Start Page

  • 785
  • End Page

  • 793
  • Volume

  • 30
  • Issue

  • 6