Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex

Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system. Investigations have mainly focused on the spinal mechanisms of neuropathic pain, and less is known about cortical changes in neuropathic pain. Here, we report that peripheral nerve injury triggered long-term changes...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:The Journal of neuroscience 2008-07, Vol.28 (29), p.7445-7453
Hauptverfasser: Xu, Hui, Wu, Long-Jun, Wang, Hansen, Zhang, Xuehan, Vadakkan, Kunjumon I, Kim, Susan S, Steenland, Hendrik W, Zhuo, Min
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 7453
container_issue 29
container_start_page 7445
container_title The Journal of neuroscience
container_volume 28
creator Xu, Hui
Wu, Long-Jun
Wang, Hansen
Zhang, Xuehan
Vadakkan, Kunjumon I
Kim, Susan S
Steenland, Hendrik W
Zhuo, Min
description Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system. Investigations have mainly focused on the spinal mechanisms of neuropathic pain, and less is known about cortical changes in neuropathic pain. Here, we report that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC). Both the presynaptic release probability of glutamate and postsynaptic glutamate AMPA receptor-mediated responses were enhanced after injury using the mouse peripheral nerve injury model. Western blot showed upregulated phosphorylation of GluR1 in the ACC after nerve injury. Finally, we found that both presynaptic and postsynaptic changes after nerve injury were absent in genetic mice lacking calcium-stimulated adenylyl cyclase 1 (AC1). Our studies therefore provide direct integrative evidence for both long-term presynaptic and postsynaptic changes in cortical synapses after nerve injury, and that AC1 is critical for such long-term changes. AC1 thus may serve as a potential therapeutic target for treating neuropathic pain.
doi_str_mv 10.1523/JNEUROSCI.1812-08.2008
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3844787</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69318222</sourcerecordid><originalsourceid>FETCH-LOGICAL-c563t-89143256fcadd54cd82c44544098e3b31be9d46119f9f57d8dfe64d6ce8157533</originalsourceid><addsrcrecordid>eNpVkV1v0zAYRi0EYmXwF6ZcwVWKvxI7N0hVtMHQtFUbuzau7TRGiR1sh7J_j6tW3ZAsWfJz3seWDwAXCC5Rhcnn77eXj_d3D-31EnGES8iXGEL-Cixy2pSYQvQaLCBmsKwpo2fgXYy_IIQMIvYWnCFeE9xQvgA_18HEJyenZFUhnS7WPqbTwWqcBttZJZP1Lha-K27NHPwkU5_TtbSuyCv1pli5ZIL1oWit286DTKZofUjm73vwppNDNB-O-zl4vLr80X4rb-6-Xrerm1JVNUklbxAluKo7JbWuqNIcK0orSmHDDdkQtDGNpjVCTdd0FdNcd6amulaGo4pVhJyDL4fead6MRivjUpCDmIIdZXgSXlrxf-JsL7b-jyCcUsZZLvh4LAj-92xiEqONygyDdMbPUdQNQRxjnMH6AKrgYwymO12CoNjLESc5Yi9HQC72cvLgxcsnPo8dbWTg0wHo7bbf2WBEHOUwZByJ3W6Hc08jWP4W8g9yCZvz</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>69318222</pqid></control><display><type>article</type><title>Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Xu, Hui ; Wu, Long-Jun ; Wang, Hansen ; Zhang, Xuehan ; Vadakkan, Kunjumon I ; Kim, Susan S ; Steenland, Hendrik W ; Zhuo, Min</creator><creatorcontrib>Xu, Hui ; Wu, Long-Jun ; Wang, Hansen ; Zhang, Xuehan ; Vadakkan, Kunjumon I ; Kim, Susan S ; Steenland, Hendrik W ; Zhuo, Min</creatorcontrib><description>Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system. Investigations have mainly focused on the spinal mechanisms of neuropathic pain, and less is known about cortical changes in neuropathic pain. Here, we report that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC). Both the presynaptic release probability of glutamate and postsynaptic glutamate AMPA receptor-mediated responses were enhanced after injury using the mouse peripheral nerve injury model. Western blot showed upregulated phosphorylation of GluR1 in the ACC after nerve injury. Finally, we found that both presynaptic and postsynaptic changes after nerve injury were absent in genetic mice lacking calcium-stimulated adenylyl cyclase 1 (AC1). Our studies therefore provide direct integrative evidence for both long-term presynaptic and postsynaptic changes in cortical synapses after nerve injury, and that AC1 is critical for such long-term changes. AC1 thus may serve as a potential therapeutic target for treating neuropathic pain.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/JNEUROSCI.1812-08.2008</identifier><identifier>PMID: 18632948</identifier><language>eng</language><publisher>United States: Soc Neuroscience</publisher><subject>Animals ; Behavior, Animal - physiology ; Disease Models, Animal ; Excitatory Postsynaptic Potentials - genetics ; Excitatory Postsynaptic Potentials - physiology ; Gyrus Cinguli - physiology ; Ligation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Pain - genetics ; Pain - physiopathology ; Peroneal Nerve ; Presynaptic Terminals - physiology ; Synaptic Transmission - genetics ; Synaptic Transmission - physiology</subject><ispartof>The Journal of neuroscience, 2008-07, Vol.28 (29), p.7445-7453</ispartof><rights>Copyright © 2008 Society for Neuroscience 0270-6474/08/287445-09$15.00/0 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c563t-89143256fcadd54cd82c44544098e3b31be9d46119f9f57d8dfe64d6ce8157533</citedby><cites>FETCH-LOGICAL-c563t-89143256fcadd54cd82c44544098e3b31be9d46119f9f57d8dfe64d6ce8157533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3844787/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3844787/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18632948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Hui</creatorcontrib><creatorcontrib>Wu, Long-Jun</creatorcontrib><creatorcontrib>Wang, Hansen</creatorcontrib><creatorcontrib>Zhang, Xuehan</creatorcontrib><creatorcontrib>Vadakkan, Kunjumon I</creatorcontrib><creatorcontrib>Kim, Susan S</creatorcontrib><creatorcontrib>Steenland, Hendrik W</creatorcontrib><creatorcontrib>Zhuo, Min</creatorcontrib><title>Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system. Investigations have mainly focused on the spinal mechanisms of neuropathic pain, and less is known about cortical changes in neuropathic pain. Here, we report that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC). Both the presynaptic release probability of glutamate and postsynaptic glutamate AMPA receptor-mediated responses were enhanced after injury using the mouse peripheral nerve injury model. Western blot showed upregulated phosphorylation of GluR1 in the ACC after nerve injury. Finally, we found that both presynaptic and postsynaptic changes after nerve injury were absent in genetic mice lacking calcium-stimulated adenylyl cyclase 1 (AC1). Our studies therefore provide direct integrative evidence for both long-term presynaptic and postsynaptic changes in cortical synapses after nerve injury, and that AC1 is critical for such long-term changes. AC1 thus may serve as a potential therapeutic target for treating neuropathic pain.</description><subject>Animals</subject><subject>Behavior, Animal - physiology</subject><subject>Disease Models, Animal</subject><subject>Excitatory Postsynaptic Potentials - genetics</subject><subject>Excitatory Postsynaptic Potentials - physiology</subject><subject>Gyrus Cinguli - physiology</subject><subject>Ligation</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Pain - genetics</subject><subject>Pain - physiopathology</subject><subject>Peroneal Nerve</subject><subject>Presynaptic Terminals - physiology</subject><subject>Synaptic Transmission - genetics</subject><subject>Synaptic Transmission - physiology</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkV1v0zAYRi0EYmXwF6ZcwVWKvxI7N0hVtMHQtFUbuzau7TRGiR1sh7J_j6tW3ZAsWfJz3seWDwAXCC5Rhcnn77eXj_d3D-31EnGES8iXGEL-Cixy2pSYQvQaLCBmsKwpo2fgXYy_IIQMIvYWnCFeE9xQvgA_18HEJyenZFUhnS7WPqbTwWqcBttZJZP1Lha-K27NHPwkU5_TtbSuyCv1pli5ZIL1oWit286DTKZofUjm73vwppNDNB-O-zl4vLr80X4rb-6-Xrerm1JVNUklbxAluKo7JbWuqNIcK0orSmHDDdkQtDGNpjVCTdd0FdNcd6amulaGo4pVhJyDL4fead6MRivjUpCDmIIdZXgSXlrxf-JsL7b-jyCcUsZZLvh4LAj-92xiEqONygyDdMbPUdQNQRxjnMH6AKrgYwymO12CoNjLESc5Yi9HQC72cvLgxcsnPo8dbWTg0wHo7bbf2WBEHOUwZByJ3W6Hc08jWP4W8g9yCZvz</recordid><startdate>20080716</startdate><enddate>20080716</enddate><creator>Xu, Hui</creator><creator>Wu, Long-Jun</creator><creator>Wang, Hansen</creator><creator>Zhang, Xuehan</creator><creator>Vadakkan, Kunjumon I</creator><creator>Kim, Susan S</creator><creator>Steenland, Hendrik W</creator><creator>Zhuo, Min</creator><general>Soc Neuroscience</general><general>Society for Neuroscience</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20080716</creationdate><title>Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex</title><author>Xu, Hui ; Wu, Long-Jun ; Wang, Hansen ; Zhang, Xuehan ; Vadakkan, Kunjumon I ; Kim, Susan S ; Steenland, Hendrik W ; Zhuo, Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c563t-89143256fcadd54cd82c44544098e3b31be9d46119f9f57d8dfe64d6ce8157533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Behavior, Animal - physiology</topic><topic>Disease Models, Animal</topic><topic>Excitatory Postsynaptic Potentials - genetics</topic><topic>Excitatory Postsynaptic Potentials - physiology</topic><topic>Gyrus Cinguli - physiology</topic><topic>Ligation</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Pain - genetics</topic><topic>Pain - physiopathology</topic><topic>Peroneal Nerve</topic><topic>Presynaptic Terminals - physiology</topic><topic>Synaptic Transmission - genetics</topic><topic>Synaptic Transmission - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Hui</creatorcontrib><creatorcontrib>Wu, Long-Jun</creatorcontrib><creatorcontrib>Wang, Hansen</creatorcontrib><creatorcontrib>Zhang, Xuehan</creatorcontrib><creatorcontrib>Vadakkan, Kunjumon I</creatorcontrib><creatorcontrib>Kim, Susan S</creatorcontrib><creatorcontrib>Steenland, Hendrik W</creatorcontrib><creatorcontrib>Zhuo, Min</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Hui</au><au>Wu, Long-Jun</au><au>Wang, Hansen</au><au>Zhang, Xuehan</au><au>Vadakkan, Kunjumon I</au><au>Kim, Susan S</au><au>Steenland, Hendrik W</au><au>Zhuo, Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>2008-07-16</date><risdate>2008</risdate><volume>28</volume><issue>29</issue><spage>7445</spage><epage>7453</epage><pages>7445-7453</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system. Investigations have mainly focused on the spinal mechanisms of neuropathic pain, and less is known about cortical changes in neuropathic pain. Here, we report that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC). Both the presynaptic release probability of glutamate and postsynaptic glutamate AMPA receptor-mediated responses were enhanced after injury using the mouse peripheral nerve injury model. Western blot showed upregulated phosphorylation of GluR1 in the ACC after nerve injury. Finally, we found that both presynaptic and postsynaptic changes after nerve injury were absent in genetic mice lacking calcium-stimulated adenylyl cyclase 1 (AC1). Our studies therefore provide direct integrative evidence for both long-term presynaptic and postsynaptic changes in cortical synapses after nerve injury, and that AC1 is critical for such long-term changes. AC1 thus may serve as a potential therapeutic target for treating neuropathic pain.</abstract><cop>United States</cop><pub>Soc Neuroscience</pub><pmid>18632948</pmid><doi>10.1523/JNEUROSCI.1812-08.2008</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0270-6474
ispartof The Journal of neuroscience, 2008-07, Vol.28 (29), p.7445-7453
issn 0270-6474
1529-2401
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3844787
source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central
subjects Animals
Behavior, Animal - physiology
Disease Models, Animal
Excitatory Postsynaptic Potentials - genetics
Excitatory Postsynaptic Potentials - physiology
Gyrus Cinguli - physiology
Ligation
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Pain - genetics
Pain - physiopathology
Peroneal Nerve
Presynaptic Terminals - physiology
Synaptic Transmission - genetics
Synaptic Transmission - physiology
title Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-05T14%3A42%3A04IST&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=Presynaptic%20and%20Postsynaptic%20Amplifications%20of%20Neuropathic%20Pain%20in%20the%20Anterior%20Cingulate%20Cortex&rft.jtitle=The%20Journal%20of%20neuroscience&rft.au=Xu,%20Hui&rft.date=2008-07-16&rft.volume=28&rft.issue=29&rft.spage=7445&rft.epage=7453&rft.pages=7445-7453&rft.issn=0270-6474&rft.eissn=1529-2401&rft_id=info:doi/10.1523/JNEUROSCI.1812-08.2008&rft_dat=%3Cproquest_pubme%3E69318222%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=69318222&rft_id=info:pmid/18632948&rfr_iscdi=true