Huntington's disease and its animal model: Alterations in kainic acid binding
Life SciencesPublished 1 February 1979
Kevin Beaumont, Yves Maurin, Terry Reisine, Jeremy Z. Fields, Ernest G. Spokes, Edward D. Bird
Citations44
SJR quartileQ1
SJR score1.31
SNIP1.07
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TL;DR
The findings confirm the validity of the KA-lesioned model for HD and suggest a post-synaptic location for kainic acid receptors in the striatum.
Abstract
The density of 3H-kainic acid (KA) binding was determined in several regions of Huntington's Diseased (HD) and control human brains. 3H-Kainic acid binding was significantly reduced by 55% in the caudate nucleus and by 53% in the putamen of HD brains. In addition, 3H-KA binding was determined in rat striatum at various intervals following lesion with KA, a procedure which produces an animal model of HD. After KA lesion, 3H-KA binding in the rat striatum underwent a slow reduction, reaching 25% of control after 6 weeks. Several properties of 3H-KA binding to rat brain membranes were also investigated, including inhibition by ions, regional distribution and displacement by various compounds. The findings confirm the validity of the KA-lesioned model for HD and suggest a post-synaptic location for kainic acid receptors in the striatum.
Keywords
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