Literature DB >> 18423442

The use of the hippocampal slice preparation in the study of Alzheimer's disease.

Stephen M Fitzjohn1, Andrew J Doherty, Graham L Collingridge.   

Abstract

In the present article we show how studying synaptic mechanisms in hippocampal slice preparations provides information that may be useful in, firstly, the understanding of the aetiology of Alzheimer's disease and, secondly, in the development of novel therapies for dementia. We use several examples, drawn from our own work: (i) The identification of the function of AMPA receptors and NMDA receptors in synaptic transmission and synaptic plasticity. (ii) The discovery of mechanisms that can regulate the activation of NMDA receptors. (iii) The use of transgenic models of Alzheimer's disease. (iv) The identification of a mechanism that can account for the cognitive enhancing effects of the NMDA receptor antagonist memantine. (v) The discovery of a role of glycogen synthase kinase-3beta (tau kinase) in synaptic plasticity.

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Year:  2008        PMID: 18423442     DOI: 10.1016/j.ejphar.2008.02.077

Source DB:  PubMed          Journal:  Eur J Pharmacol        ISSN: 0014-2999            Impact factor:   4.432


  10 in total

Review 1.  Synapses and Alzheimer's disease.

Authors:  Morgan Sheng; Bernardo L Sabatini; Thomas C Südhof
Journal:  Cold Spring Harb Perspect Biol       Date:  2012-05-01       Impact factor: 10.005

2.  Induction of apoptotic change in the rat hippocampus caused by ferric nitrilotriacetate.

Authors:  Shigeru Maeda; Yukiko Arai; Hitoshi Higuchi; Yumiko Tomoyasu; Ryuichiro Mizuno; Toru Takahashi; Takuya Miyawaki
Journal:  Redox Rep       Date:  2011       Impact factor: 4.412

Review 3.  Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.

Authors:  Dezhi Liao; Eric C Miller; Peter J Teravskis
Journal:  Eur J Neurosci       Date:  2014-04       Impact factor: 3.386

Review 4.  The NMDA receptor as a target for cognitive enhancement.

Authors:  Graham L Collingridge; Arturas Volianskis; Neil Bannister; Grace France; Lydia Hanna; Marion Mercier; Patrick Tidball; Guangyu Fang; Mark W Irvine; Blaise M Costa; Daniel T Monaghan; Zuner A Bortolotto; Elek Molnár; David Lodge; David E Jane
Journal:  Neuropharmacology       Date:  2012-07-11       Impact factor: 5.250

5.  A study of long-term potentiation in transgenic mice over-expressing mutant forms of both amyloid precursor protein and presenilin-1.

Authors:  Stephen M Fitzjohn; Frederick Kuenzi; Robin A Morton; Thomas W Rosahl; Huw Lewis; David Smith; Guy R Seabrook; Graham L Collingridge
Journal:  Mol Brain       Date:  2010-07-14       Impact factor: 4.041

6.  Characterization of altered intrinsic excitability in hippocampal CA1 pyramidal cells of the Aβ-overproducing PDAPP mouse.

Authors:  T L Kerrigan; J T Brown; A D Randall
Journal:  Neuropharmacology       Date:  2013-09-18       Impact factor: 5.250

7.  Intrinsic excitability changes induced by acute treatment of hippocampal CA1 pyramidal neurons with exogenous amyloid β peptide.

Authors:  Francesco Tamagnini; Sarah Scullion; Jon T Brown; Andrew D Randall
Journal:  Hippocampus       Date:  2015-03-25       Impact factor: 3.899

8.  Short-term dynamics of input and output of CA1 network greatly differ between the dorsal and ventral rat hippocampus.

Authors:  Andriana Koutsoumpa; Costas Papatheodoropoulos
Journal:  BMC Neurosci       Date:  2019-07-22       Impact factor: 3.288

9.  Amyloid-β(25-35) Modulates the Expression of GirK and KCNQ Channel Genes in the Hippocampus.

Authors:  Jennifer Mayordomo-Cava; Javier Yajeya; Juan D Navarro-López; Lydia Jiménez-Díaz
Journal:  PLoS One       Date:  2015-07-28       Impact factor: 3.240

Review 10.  Organotypic brain slice cultures to model neurodegenerative proteinopathies.

Authors:  C L Croft; H S Futch; B D Moore; T E Golde
Journal:  Mol Neurodegener       Date:  2019-12-02       Impact factor: 14.195

  10 in total

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