Regional distribution of pre- and postsynaptic glutamatergic function in Alzheimer's disease.
Ca2+/Cl- -independent L-[3H]glutamate- and sodium-dependent D-[3H]aspartate binding assays were used to assess the integrity of N-methyl-D-aspartate (NMDA) receptors and glutamate uptake sites in a number of areas from control and Alzheimer's diseased brain. NMDA receptor densities were unchanged in all areas tested. In contrast, significant reductions in the number of glutamate terminals were seen in the hippocampus of the Alzheimer's samples. A smaller reduction was seen in the caudate nucleus but this failed to reach significance. No such reductions were seen in either the frontal or parietal cortices.
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism*; D001224:Aspartic Acid / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D002421:Caudate Nucleus / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D005260:Female; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D006624:Hippocampus / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D008297:Male; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000378:metabolism*
D005971:Glutamates; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D001224:Aspartic Acid; D018698:Glutamic Acid