Neuronal and peripheral pentraxins modify glutamate release and may interact in blood-brain barrier failure

Cummings, Damian M., Benway, Tiffanie A., Ho, Hinze, Tedoldi, Angelo, Freitas, Monica M. Fernandes, Shahab, Lion, Murray, Christina E., Richard-Loendt, Angela, Brandner, Sebastian, Lashley, Tammaryn, Salih, Dervis A. and Edwards, Frances A. (2017) Neuronal and peripheral pentraxins modify glutamate release and may interact in blood-brain barrier failure. Cerebral Cortex, 27 6: 3437-3448. doi:10.1093/cercor/bhx046


Author Cummings, Damian M.
Benway, Tiffanie A.
Ho, Hinze
Tedoldi, Angelo
Freitas, Monica M. Fernandes
Shahab, Lion
Murray, Christina E.
Richard-Loendt, Angela
Brandner, Sebastian
Lashley, Tammaryn
Salih, Dervis A.
Edwards, Frances A.
Title Neuronal and peripheral pentraxins modify glutamate release and may interact in blood-brain barrier failure
Journal name Cerebral Cortex   Check publisher's open access policy
ISSN 1047-3211
1460-2199
Publication date 2017-06-01
Year available 2017
Sub-type Article (original research)
DOI 10.1093/cercor/bhx046
Open Access Status DOI
Volume 27
Issue 6
Start page 3437
End page 3448
Total pages 12
Place of publication Oxford, United Kingdom
Publisher Oxford University Press
Language eng
Subject 2805 Cognitive Neuroscience
2804 Cellular and Molecular Neuroscience
Abstract Neuronal pentraxin 1 (NPTX1) has been implicated in Alzheimer's disease, being present in and around dystrophic neurons in plaques, affecting glutamatergic transmission postsynaptically and mediating effects of amyloidβ. Here, we confirm the presence of NPTX1 around plaques in postmortem Alzheimer's disease brain and report that acutely applied human NPTX1 increases paired-pulse ratio at mouse CA3-CA1 hippocampal synapses, indicating a decrease in glutamate release. In contrast, chronic exposure to NPTX1, NPTX2, or NPTX receptor decreases paired-pulse ratio, mimicking some of the earliest changes in mice expressing familial Alzheimer's disease genes. The peripheral pentraxin, serum amyloid P component (SAP), causes similar synaptic effects to NPTX1. The presence of SAP on amyloid plaques in Alzheimer's disease confirms that it can enter the brain. We show that SAP and neuronal pentraxins can interact and that SAP can enter the brain if the blood–brain barrier is compromised, suggesting that peripheral pentraxins could affect central synaptic transmission via this interaction, especially in the event of blood–brain barrier breakdown.
Keyword Alzheimer's disease
Central nervous system
Neurodegenerative disease
Presynaptic
Synaptic plasticity
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID MR/J011851/1
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
Queensland Brain Institute Publications
 
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