Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Science 22 March 1985:
Vol. 227. no. 4693, pp. 1496 - 1499
DOI: 10.1126/science.2858129
Prev | Table of Contents | Next

Articles

Science, Vol 227, Issue 4693, 1496-1499
Copyright © 1985 by American Association for the Advancement of Science

articles

Alterations in L-glutamate binding in Alzheimer's and Huntington's diseases

JT Greenamyre, JB Penney, AB Young, CJ D'Amato, SP Hicks, and I Shoulson

Brain sections from patients who had died with senile dementia of the Alzheimer's type (SDAT), Huntington's disease (HD), or no neurologic disease were studied by autoradiography to measure sodium-independent L-[3H]glutamate binding. In brain sections from SDAT patients, glutamate binding was normal in the caudate, putamen, and claustrum but was lower than normal in the cortex. The decreased cortical binding represented a reduction in numbers of binding sites, not a change in binding affinity, and appeared to be the result of a specific decrease in numbers of the low-affinity quisqualate binding site. No significant changes in cortical binding of other ligands were observed. In brains from Huntington's disease patients, glutamate binding was lower in the caudate and putamen than in the same regions of brains from control and SDAT patients but was normal in the cortex. It is possible that development of positron-emitting probes for glutamate receptors may permit diagnosis of SDAT in vivo by means of positron emission tomographic scanning.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Paradoxical Upregulation of Glutamatergic Presynaptic Boutons during Mild Cognitive Impairment.
K. F. S. Bell, D. A. Bennett, and A. C. Cuello (2007)
J. Neurosci. 27, 10810-10817
   Abstract »    Full Text »    PDF »
Neuroanatomy/pathology and the interplay of neurotransmitters in moderate to severe Alzheimer disease.
P. T. Francis (2005)
Neurology 65, S5-S9
   Full Text »
Estrogen Receptor-Mediated Neuroprotection from Oxidative Stress Requires Activation of the Mitogen-Activated Protein Kinase Pathway.
A. L. Mize, R. A. Shapiro, and D. M. Dorsa (2003)
Endocrinology 144, 306-312
   Abstract »    Full Text »    PDF »
Persistent Activation of ERK Contributes to Glutamate-induced Oxidative Toxicity in a Neuronal Cell Line and Primary Cortical Neuron Cultures.
M. Stanciu, Y. Wang, R. Kentor, N. Burke, S. Watkins, G. Kress, I. Reynolds, E. Klann, M. R. Angiolieri, J. W. Johnson, et al. (2000)
J. Biol. Chem. 275, 12200-12206
   Abstract »    Full Text »    PDF »
The Role of Monoamine Metabolism in Oxidative Glutamate Toxicity.
P. Maher and J. B. Davis (1996)
J. Neurosci. 16, 6394-6401
   Abstract »    Full Text »    PDF »
{blacksquare} REVIEW : Glutamate Receptors: Emerging Links Between Subunit Proteins and Specific Excitatory Circuits in Primate Hippocampus and Neocortex.
J. H. Morrison, S. J. Siegel, A. H. Gazzaley, and G. W. Huntley (1996)
Neuroscientist 2, 272-283
   Abstract »    PDF »
Neurotrophic Factor Protection against Excitotoxic Neuronal Death.
S. B. Tatter, W. R. Galpern, and O. Isacson (1995)
Neuroscientist 1, 286-297
   Abstract »    PDF »
NMDA receptor losses in putamen from patients with Huntington's disease.
A. Young, J. Greenamyre, Z Hollingsworth, R Albin, C D'Amato, I Shoulson, and J. Penney (1988)
Science 241, 981-983
   Abstract »    PDF »
Reductions in Acetylcholine and Nicotine Binding in Several Degenerative Diseases.
P. J. Whitehouse, A. M. Martino, K. A. Marcus, R. M. Zweig, H. S. Singer, D. L. Price, and K. J. Kellar (1988)
Arch Neurol 45, 722-724
   Abstract »    PDF »
Bilateral Symmetry of Cholinergic Deficits in Alzheimer's Disease.
G. S. Zubenko, J. Moossy, I. Hanin, A. J. Martinez, G. R. Rao, and U. Kopp (1988)
Arch Neurol 45, 255-259
   Abstract »    PDF »
Perspectives on the Etiology of Alzheimer's Disease.
H. N. Mozar, D. G. Bal, and J. T. Howard (1987)
JAMA 257, 1503-1507
   Abstract »    PDF »
The Role of Glutamate in Neurotransmission and in Neurologic Disease.
J. T. Greenamyre (1986)
Arch Neurol 43, 1058-1063
   Abstract »    PDF »
Plasticity of hippocampal circuitry in Alzheimer's disease.
J. Geddes, D. Monaghan, C. Cotman, I. Lott, R. Kim, and H. Chui (1985)
Science 230, 1179-1181
   Abstract »    PDF »


To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)