Plasticity in hippocampal excitatory amino acid receptors in Alzheimer's disease.

Entorhinal cell loss occurs in the course of Alzheimer's disease. In rodents, entorhinal lesions result in axon sprouting in the hippocampus. Quantitative autoradiography was used to examine the density and distribution of N-methyl-D-aspartate (NMDA) and kainic acid (KA) receptors in human hippocampus obtained post-mortem from Alzheimer's disease patients and from age-matched controls. In Alzheimer's disease, there was an expanded distribution of the KA receptor field in the dentate gyrus, indicative of sprouting of the commissural and associational fibers. This regenerative response is thought to facilitate transmission, but in doing so it may also enhance vulnerability to excitotoxic mediated neuronal damage. No significant change was observed in the density or distribution of NMDA receptors. The distribution of these receptors does, however, correlate with the predilection for neurofibrillary tangles and neuritic plaques in hippocampal subfields.