Loading…

β-amyloid inhibits hippocampal LTP through TNFR/IKK/NF-κB pathway

The suppressive action of the acute application of oligomeric amyloid-β (Aβ) on hippocampal long-term potentiation (LTP) has been reported widely. Many mechanisms have been proposed for Aβ inhibited LTP induction. The inflammatory cytokine tumor necrosis factor-α (TNF-α) has also been reported to pl...

Full description

Saved in:
Bibliographic Details
Published in:Neurological research (New York) 2018-04, Vol.40 (4), p.268-276
Main Authors: Samidurai, Manikandan, Ramasamy, Vijay S., Jo, Jihoon
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c366t-8be4c0e9dd5c1d5c7cd10d173d19e31e4e521937f376be8e46208b4561f6e1fa3
cites cdi_FETCH-LOGICAL-c366t-8be4c0e9dd5c1d5c7cd10d173d19e31e4e521937f376be8e46208b4561f6e1fa3
container_end_page 276
container_issue 4
container_start_page 268
container_title Neurological research (New York)
container_volume 40
creator Samidurai, Manikandan
Ramasamy, Vijay S.
Jo, Jihoon
description The suppressive action of the acute application of oligomeric amyloid-β (Aβ) on hippocampal long-term potentiation (LTP) has been reported widely. Many mechanisms have been proposed for Aβ inhibited LTP induction. The inflammatory cytokine tumor necrosis factor-α (TNF-α) has also been reported to play a key role in this LTP inhibition through Aβ. However, the underlying molecular mechanisms are largely unknown. This study aimed to investigate the link between Aβ- and TNF-α-mediated hippocampal LTP inhibition. Acute hippocampal slices of male wildtype or Alzheimer's disease (AD) transgenic mouse models were treated with the inhibitors of either TNF-α, IκB Kinase (IKK) or Nuclear Factor-κB (NF-κB) in the presence or absence of oligomeric Aβ 42 (500 nM/2 h). The LTP was assessed using field excitatory post synaptic potential recordings (fEPSP), and immunoblotting was used to evaluate the expression of IKK and NF-κB. Acute treatment with Aβ or TNF-α alone inhibited LTP and increased the phosphorylation of IKK and NF-κB in wild type mouse hippocampal slices. Pretreatment with TNF-α antagonist infliximab rescued the LTP impairment by Aβ and also restored the levels of IKK and NF-κB to the control levels. In addition, pretreatment with IKK2 IV or JSH23 also restored the Aβ-mediated LTP impairment. Furthermore, AD transgenic mouse hippocampal slices treated with infliximab or inhibitors of IKK or NF-κB showed improved LTP and reversed the activation of IKK and NF-κB. In conclusion, our observations suggest that the IKK/NF-κB signaling pathway play an important role in Aβ-mediated hippocampal LTP impairment. Aβ might modulate IKK/NF-κB activity by binding or activating tumor necrosis factor receptor (TNFR).
doi_str_mv 10.1080/01616412.2018.1436872
format article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmed_primary_29458298</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2007114231</sourcerecordid><originalsourceid>FETCH-LOGICAL-c366t-8be4c0e9dd5c1d5c7cd10d173d19e31e4e521937f376be8e46208b4561f6e1fa3</originalsourceid><addsrcrecordid>eNp9kLFOwzAURS0EoqXwCaCMLGn9bMdxNqCiULUqCJXZchKHGCVNsBNV_S1GPqLfRKq2jAxPbzn3XukgdA14CFjgEQYOnAEZEgxiCIxyEZIT1IeQUR8oEaeov2P8HdRDF859YgwREdE56pGIBYJEoo_G229flZuiMqlnVrmJTeO83NR1laiyVoU3X756TW6r9iP3lovJ22g6m40WE3_78-DVqsnXanOJzjJVOH11-AP0Pnlcjp_9-cvTdHw_9xPKeeOLWLME6yhNgwS6C5MUcAohTSHSFDTTAYGIhhkNeayFZpxgEbOAQ8Y1ZIoO0O2-t7bVV6tdI0vjEl0UaqWr1kmCcQjACIUODfZoYivnrM5kbU2p7EYCljt_8uhP7vzJg78ud3OYaONSp3-po7AOuNsDZpVVtlTryhapbFRn0GZWrRLjJP1_4xdDt36o</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2007114231</pqid></control><display><type>article</type><title>β-amyloid inhibits hippocampal LTP through TNFR/IKK/NF-κB pathway</title><source>Taylor and Francis:Jisc Collections:Taylor and Francis Read and Publish Agreement 2024-2025:Medical Collection (Reading list)</source><creator>Samidurai, Manikandan ; Ramasamy, Vijay S. ; Jo, Jihoon</creator><creatorcontrib>Samidurai, Manikandan ; Ramasamy, Vijay S. ; Jo, Jihoon</creatorcontrib><description>The suppressive action of the acute application of oligomeric amyloid-β (Aβ) on hippocampal long-term potentiation (LTP) has been reported widely. Many mechanisms have been proposed for Aβ inhibited LTP induction. The inflammatory cytokine tumor necrosis factor-α (TNF-α) has also been reported to play a key role in this LTP inhibition through Aβ. However, the underlying molecular mechanisms are largely unknown. This study aimed to investigate the link between Aβ- and TNF-α-mediated hippocampal LTP inhibition. Acute hippocampal slices of male wildtype or Alzheimer's disease (AD) transgenic mouse models were treated with the inhibitors of either TNF-α, IκB Kinase (IKK) or Nuclear Factor-κB (NF-κB) in the presence or absence of oligomeric Aβ 42 (500 nM/2 h). The LTP was assessed using field excitatory post synaptic potential recordings (fEPSP), and immunoblotting was used to evaluate the expression of IKK and NF-κB. Acute treatment with Aβ or TNF-α alone inhibited LTP and increased the phosphorylation of IKK and NF-κB in wild type mouse hippocampal slices. Pretreatment with TNF-α antagonist infliximab rescued the LTP impairment by Aβ and also restored the levels of IKK and NF-κB to the control levels. In addition, pretreatment with IKK2 IV or JSH23 also restored the Aβ-mediated LTP impairment. Furthermore, AD transgenic mouse hippocampal slices treated with infliximab or inhibitors of IKK or NF-κB showed improved LTP and reversed the activation of IKK and NF-κB. In conclusion, our observations suggest that the IKK/NF-κB signaling pathway play an important role in Aβ-mediated hippocampal LTP impairment. Aβ might modulate IKK/NF-κB activity by binding or activating tumor necrosis factor receptor (TNFR).</description><identifier>ISSN: 0161-6412</identifier><identifier>EISSN: 1743-1328</identifier><identifier>DOI: 10.1080/01616412.2018.1436872</identifier><identifier>PMID: 29458298</identifier><language>eng</language><publisher>England: Taylor &amp; Francis</publisher><subject>Alzheimer's disease ; LTP ; TNF-α ; β-amyloid</subject><ispartof>Neurological research (New York), 2018-04, Vol.40 (4), p.268-276</ispartof><rights>2018 Informa UK Limited, trading as Taylor &amp; Francis Group 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c366t-8be4c0e9dd5c1d5c7cd10d173d19e31e4e521937f376be8e46208b4561f6e1fa3</citedby><cites>FETCH-LOGICAL-c366t-8be4c0e9dd5c1d5c7cd10d173d19e31e4e521937f376be8e46208b4561f6e1fa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29458298$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Samidurai, Manikandan</creatorcontrib><creatorcontrib>Ramasamy, Vijay S.</creatorcontrib><creatorcontrib>Jo, Jihoon</creatorcontrib><title>β-amyloid inhibits hippocampal LTP through TNFR/IKK/NF-κB pathway</title><title>Neurological research (New York)</title><addtitle>Neurol Res</addtitle><description>The suppressive action of the acute application of oligomeric amyloid-β (Aβ) on hippocampal long-term potentiation (LTP) has been reported widely. Many mechanisms have been proposed for Aβ inhibited LTP induction. The inflammatory cytokine tumor necrosis factor-α (TNF-α) has also been reported to play a key role in this LTP inhibition through Aβ. However, the underlying molecular mechanisms are largely unknown. This study aimed to investigate the link between Aβ- and TNF-α-mediated hippocampal LTP inhibition. Acute hippocampal slices of male wildtype or Alzheimer's disease (AD) transgenic mouse models were treated with the inhibitors of either TNF-α, IκB Kinase (IKK) or Nuclear Factor-κB (NF-κB) in the presence or absence of oligomeric Aβ 42 (500 nM/2 h). The LTP was assessed using field excitatory post synaptic potential recordings (fEPSP), and immunoblotting was used to evaluate the expression of IKK and NF-κB. Acute treatment with Aβ or TNF-α alone inhibited LTP and increased the phosphorylation of IKK and NF-κB in wild type mouse hippocampal slices. Pretreatment with TNF-α antagonist infliximab rescued the LTP impairment by Aβ and also restored the levels of IKK and NF-κB to the control levels. In addition, pretreatment with IKK2 IV or JSH23 also restored the Aβ-mediated LTP impairment. Furthermore, AD transgenic mouse hippocampal slices treated with infliximab or inhibitors of IKK or NF-κB showed improved LTP and reversed the activation of IKK and NF-κB. In conclusion, our observations suggest that the IKK/NF-κB signaling pathway play an important role in Aβ-mediated hippocampal LTP impairment. Aβ might modulate IKK/NF-κB activity by binding or activating tumor necrosis factor receptor (TNFR).</description><subject>Alzheimer's disease</subject><subject>LTP</subject><subject>TNF-α</subject><subject>β-amyloid</subject><issn>0161-6412</issn><issn>1743-1328</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kLFOwzAURS0EoqXwCaCMLGn9bMdxNqCiULUqCJXZchKHGCVNsBNV_S1GPqLfRKq2jAxPbzn3XukgdA14CFjgEQYOnAEZEgxiCIxyEZIT1IeQUR8oEaeov2P8HdRDF859YgwREdE56pGIBYJEoo_G229flZuiMqlnVrmJTeO83NR1laiyVoU3X756TW6r9iP3lovJ22g6m40WE3_78-DVqsnXanOJzjJVOH11-AP0Pnlcjp_9-cvTdHw_9xPKeeOLWLME6yhNgwS6C5MUcAohTSHSFDTTAYGIhhkNeayFZpxgEbOAQ8Y1ZIoO0O2-t7bVV6tdI0vjEl0UaqWr1kmCcQjACIUODfZoYivnrM5kbU2p7EYCljt_8uhP7vzJg78ud3OYaONSp3-po7AOuNsDZpVVtlTryhapbFRn0GZWrRLjJP1_4xdDt36o</recordid><startdate>20180403</startdate><enddate>20180403</enddate><creator>Samidurai, Manikandan</creator><creator>Ramasamy, Vijay S.</creator><creator>Jo, Jihoon</creator><general>Taylor &amp; Francis</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20180403</creationdate><title>β-amyloid inhibits hippocampal LTP through TNFR/IKK/NF-κB pathway</title><author>Samidurai, Manikandan ; Ramasamy, Vijay S. ; Jo, Jihoon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c366t-8be4c0e9dd5c1d5c7cd10d173d19e31e4e521937f376be8e46208b4561f6e1fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alzheimer's disease</topic><topic>LTP</topic><topic>TNF-α</topic><topic>β-amyloid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Samidurai, Manikandan</creatorcontrib><creatorcontrib>Ramasamy, Vijay S.</creatorcontrib><creatorcontrib>Jo, Jihoon</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurological research (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Samidurai, Manikandan</au><au>Ramasamy, Vijay S.</au><au>Jo, Jihoon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>β-amyloid inhibits hippocampal LTP through TNFR/IKK/NF-κB pathway</atitle><jtitle>Neurological research (New York)</jtitle><addtitle>Neurol Res</addtitle><date>2018-04-03</date><risdate>2018</risdate><volume>40</volume><issue>4</issue><spage>268</spage><epage>276</epage><pages>268-276</pages><issn>0161-6412</issn><eissn>1743-1328</eissn><abstract>The suppressive action of the acute application of oligomeric amyloid-β (Aβ) on hippocampal long-term potentiation (LTP) has been reported widely. Many mechanisms have been proposed for Aβ inhibited LTP induction. The inflammatory cytokine tumor necrosis factor-α (TNF-α) has also been reported to play a key role in this LTP inhibition through Aβ. However, the underlying molecular mechanisms are largely unknown. This study aimed to investigate the link between Aβ- and TNF-α-mediated hippocampal LTP inhibition. Acute hippocampal slices of male wildtype or Alzheimer's disease (AD) transgenic mouse models were treated with the inhibitors of either TNF-α, IκB Kinase (IKK) or Nuclear Factor-κB (NF-κB) in the presence or absence of oligomeric Aβ 42 (500 nM/2 h). The LTP was assessed using field excitatory post synaptic potential recordings (fEPSP), and immunoblotting was used to evaluate the expression of IKK and NF-κB. Acute treatment with Aβ or TNF-α alone inhibited LTP and increased the phosphorylation of IKK and NF-κB in wild type mouse hippocampal slices. Pretreatment with TNF-α antagonist infliximab rescued the LTP impairment by Aβ and also restored the levels of IKK and NF-κB to the control levels. In addition, pretreatment with IKK2 IV or JSH23 also restored the Aβ-mediated LTP impairment. Furthermore, AD transgenic mouse hippocampal slices treated with infliximab or inhibitors of IKK or NF-κB showed improved LTP and reversed the activation of IKK and NF-κB. In conclusion, our observations suggest that the IKK/NF-κB signaling pathway play an important role in Aβ-mediated hippocampal LTP impairment. Aβ might modulate IKK/NF-κB activity by binding or activating tumor necrosis factor receptor (TNFR).</abstract><cop>England</cop><pub>Taylor &amp; Francis</pub><pmid>29458298</pmid><doi>10.1080/01616412.2018.1436872</doi><tpages>9</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0161-6412
ispartof Neurological research (New York), 2018-04, Vol.40 (4), p.268-276
issn 0161-6412
1743-1328
language eng
recordid cdi_pubmed_primary_29458298
source Taylor and Francis:Jisc Collections:Taylor and Francis Read and Publish Agreement 2024-2025:Medical Collection (Reading list)
subjects Alzheimer's disease
LTP
TNF-α
β-amyloid
title β-amyloid inhibits hippocampal LTP through TNFR/IKK/NF-κB pathway
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-10T23%3A16%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=%CE%B2-amyloid%20inhibits%20hippocampal%20LTP%20through%20TNFR/IKK/NF-%CE%BAB%20pathway&rft.jtitle=Neurological%20research%20(New%20York)&rft.au=Samidurai,%20Manikandan&rft.date=2018-04-03&rft.volume=40&rft.issue=4&rft.spage=268&rft.epage=276&rft.pages=268-276&rft.issn=0161-6412&rft.eissn=1743-1328&rft_id=info:doi/10.1080/01616412.2018.1436872&rft_dat=%3Cproquest_pubme%3E2007114231%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c366t-8be4c0e9dd5c1d5c7cd10d173d19e31e4e521937f376be8e46208b4561f6e1fa3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2007114231&rft_id=info:pmid/29458298&rfr_iscdi=true