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Presynaptic and postsynaptic glutamatergic function in Alzheimer's disease

Presynaptic and postsynaptic glutamatergic function in Alzheimer's disease
Presynaptic and postsynaptic glutamatergic function in Alzheimer's disease

Sodium dependent d-aspartate and Ca2+ Cl- independent l-glutamate binding assays were used to assess the integrity of glutamate uptake sites and postsynaptic NMDA receptor levels in control and Alzheimer's disease temporal cortex. The number of glutamate uptake sites was significantly and substantially reduced in accordance with previous findings. However, NMDA receptor levels were unchanged. This finding suggests that glutamatergic presynaptic elements are severely reduced in Alzheimer's disease, whilst postsynaptic elements remain intact.

Alzheimer's disease, Glutamate terminal, N-Methyl-d-aspartic acid receptor, Temporal cortex
0304-3940
109-113
Cowburn, Richard
a5d9f8e5-7785-4726-9b11-9143c2c3f593
Hardy, John
bc8f3d96-0063-44a8-ad79-197befd225a6
Roberts, Peter
ab0ce3bd-e5a0-42a9-818c-ad502d7789f3
Briggs, Roger
a6b65ef0-e90c-4c07-bf5b-b70130c128b3
Cowburn, Richard
a5d9f8e5-7785-4726-9b11-9143c2c3f593
Hardy, John
bc8f3d96-0063-44a8-ad79-197befd225a6
Roberts, Peter
ab0ce3bd-e5a0-42a9-818c-ad502d7789f3
Briggs, Roger
a6b65ef0-e90c-4c07-bf5b-b70130c128b3

Cowburn, Richard, Hardy, John, Roberts, Peter and Briggs, Roger (1988) Presynaptic and postsynaptic glutamatergic function in Alzheimer's disease. Neuroscience Letters, 86 (1), 109-113. (doi:10.1016/0304-3940(88)90192-9).

Record type: Article

Abstract

Sodium dependent d-aspartate and Ca2+ Cl- independent l-glutamate binding assays were used to assess the integrity of glutamate uptake sites and postsynaptic NMDA receptor levels in control and Alzheimer's disease temporal cortex. The number of glutamate uptake sites was significantly and substantially reduced in accordance with previous findings. However, NMDA receptor levels were unchanged. This finding suggests that glutamatergic presynaptic elements are severely reduced in Alzheimer's disease, whilst postsynaptic elements remain intact.

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More information

Published date: 21 March 1988
Additional Information: Funding Information: This work was supported by grants from the Wellcome Trust (P.R. and R.B.) and by the Research Corporation Trust (J.H.). R.C. is an MRC scholar. We thank Angela Symons, Prof. R.O. Weller and Drs. B.S. Wilkins, M. Simpson, P. Slater, D.C. Davies and S.W. Davies for valuable contributions to the work.
Keywords: Alzheimer's disease, Glutamate terminal, N-Methyl-d-aspartic acid receptor, Temporal cortex

Identifiers

Local EPrints ID: 479120
URI: http://eprints.soton.ac.uk/id/eprint/479120
ISSN: 0304-3940
PURE UUID: 3c2096fc-b49d-4e52-88d7-99fc4c784811

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Date deposited: 20 Jul 2023 16:36
Last modified: 17 Mar 2024 13:24

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Contributors

Author: Richard Cowburn
Author: John Hardy
Author: Peter Roberts
Author: Roger Briggs

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