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Degeneration of pyramidal projection neurons in Huntington's disease cortex
Author(s) -
Cudkowicz Merit,
Kowall Neil W.
Publication year - 1990
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410270217
Subject(s) - quinolinic acid , huntington's disease , neuroscience , cerebral cortex , neuropeptide , neuropeptide y receptor , biology , glutamate receptor , degenerative disease , cortex (anatomy) , temporal cortex , endocrinology , medicine , central nervous system disease , receptor , disease , amino acid , tryptophan , biochemistry
We examined the distribution of neuropeptide Y immunoreactive local circuit neurons and nonphosphorylated neurofilament (SMI 32) immunoreactive pyramidal projection neurons in superior frontal cortex of patients with Huntington's disease and age‐matched control subjects to determine the histological counterpart of increased neuropeptide Y and decreased glutamate concentrations previously found in the cortex of patients with Huntington's disease. We found no difference between the relative density of neuropeptide Y neurons in Huntingon's disease and control brains in regions where the relative density of SMI 32 immunoreactive neurons was significantly reduced. Animal studies show that cortical local circuit neurons are resistant to N ‐methyl‐D‐aspartate‐type excitotoxins such as quinolinic acid. Relative sparing of neuropeptide Y neurons in cerebral cortex with Huntington's disease may, therefore, be a result of excessive N ‐methyl‐D‐asparate receptor activation.