Abstract
Journal of NeurochemistryVolume 155, Issue 1 Issue CoverFree Access Issue Cover (October 2020) First published: 30 September 2020 https://doi.org/10.1111/jnc.14763 Read the full article: ‘Amyloid-beta1–42 induced glutamatergic receptor and transporter expression changes in the mouse hippocampus’ by J. H. Y. Yeung, B. C.-F. Guzmán, T. H. Palpagama, J. Ethiraj, Y. Zhai, W. P. Tate, K. Peppercorn, H. J. Waldvogel, R. L. M. Faull, A. Kwakowsky, (J. Neurochem. 2020, vol. 155 (1), pp. 19–62) on doi:10.1111/jnc.15099 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Graphical Abstract Front cover: Alzheimer's Disease (AD) is the leading type of dementia worldwide. Glutamate is the main excitatory neurotransmitter in the brain and plays an essential role in the function and health of neurons and neuronal excitability. This is the first comprehensive anatomical study to characterize the subregion- and cell layer-specific effect of beta-amyloid (Aβ1-42) on the expression of specific glutamate receptors and transporters in the mouse hippocampus, using immunohistochemistry with confocal microscopy. Our data demonstrate heterogeneous expression changes in glutamatergic signaling components in an in vivo Aβ1-42-injected mouse model of AD. These changes have the ability to alter normal glutamatergic signaling and could contribute to AD pathology. Due to the pivotal role of the glutamatergic system in regulating synaptic activity, any disruption to its composition could have consequences for normal neuronal function. These findings also indicate that Aβ1-42 induces brain region and layer specific expression changes of the glutamatergic receptors and transporters, suggesting complex and spatial vulnerability of this pathway during AD neuropathology. Image content: The image shows glutamate receptor GluA1 subunit (green) and glutamate transporter vGluT1 (red) immunoreactivity in CA3 region of the mouse hippocampus. Nuclei were counterstained with Hoechst dye (blue). Read the full article ‘Amyloid-beta1–42 induced glutamatergic receptor and transporter expression changes in the mouse hippocampus’ by J. H. Y. Yeung, B. C.-F. Guzmán, T. H. Palpagama, J. Ethiraj, Y. Zhai, W. P. Tate, K. Peppercorn, H. J. Waldvogel, R. L. M. Faull, A. Kwakowsky, (J. Neurochem. 2020, vol. 155 (1), pp. 19–62) on doi:10.1111/jnc.15099 Volume155, Issue1October 2020 RelatedInformation
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