K
Kevin W. Kaatz
Researcher at University of Michigan
Publications - 8
Citations - 824
Kevin W. Kaatz is an academic researcher from University of Michigan. The author has contributed to research in topics: Metabotropic glutamate receptor & Metabotropic receptor. The author has an hindex of 6, co-authored 7 publications receiving 804 citations.
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Journal ArticleDOI
Widespread expression of the human and rat Huntington's disease gene in brain and nonneural tissues.
Theresa V. Strong,Danilo A. Tagle,John Valdes,Lawrence W. Elmer,Karina Boehm,Manju Swaroop,Kevin W. Kaatz,Francis S. Collins,Roger L. Albin +8 more
TL;DR: The regional specificity of neuropathology in HD, which is most prominent in the basal ganglia, thus cannot be accounted for by the pattern of expression of HD.
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Localization of mGluR1a-like immunoreactivity and mGluR5-like immunoreactivity in identified populations of striatal neurons
TL;DR: Findings indicate considerable heterogeneity among striatal projection and interneurons with respect to mGluR1a and mGLUR5 expression and there may be subpopulations of striatonigral and striatopallidal projection neurons.
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Intrastriatal and intrasubthalamic stimulation of metabotropic glutamate receptors : a behavioral and Fos immunohistochemical study
Kevin W. Kaatz,Roger L. Albin +1 more
TL;DR: Investigation of the expression of Fos-like immunoreactivity after intrastriatal injection of 1S,3R-ACPD suggests that stimulation of striatal metabotropic glutamate receptors inhibits striatal projection neuron activity, while stimulation of subthalamic metabotrop glutamate receptors increasesSubthalamic nucleus activity.
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Quisqualate- and NMDA-Sensitive (3H)Glutamate Binding in Primate Brain
Anne B. Young,George W. Dauth,Zane R. Hollingsworth,John B. Penney,Kevin W. Kaatz,Sid Gilman +5 more
TL;DR: The two types of binding were differentially distributed, and strikingly the red nucleus and pons, which are thought to receive glutamatergic projections, had approximately 1/20 the binding observed in cerebral cortex.
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Chronic Intrastriatal Dialytic Administration of Quinolinic Acid Produces Selective Neural Degeneration
TL;DR: It is concluded that dialytic delivery of 3.3 mumol quinolinic acid produces an area of neuronal destruction that resembles the selective neuronal loss seen in Huntington's disease.