The periaqueductal grey is a critical site in the neuronal network for audiogenic seizures: modulation by GABA A, NMDA and opioid receptors

The nuclei comprising the neuronal network for audiogenic seizures (AGS) are located primarily in the brainstem. Previous studies suggested a role for the periaqueductal grey (PAG) in the AGS network. The present study evaluated this possibility in genetically-epilepsy prone rats (GEPR-9s) by examin...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Epilepsy research 1999-05, Vol.35 (1), p.39-46
Hauptverfasser: N’Gouemo, Prosper, Faingold, Carl L
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 46
container_issue 1
container_start_page 39
container_title Epilepsy research
container_volume 35
creator N’Gouemo, Prosper
Faingold, Carl L
description The nuclei comprising the neuronal network for audiogenic seizures (AGS) are located primarily in the brainstem. Previous studies suggested a role for the periaqueductal grey (PAG) in the AGS network. The present study evaluated this possibility in genetically-epilepsy prone rats (GEPR-9s) by examining the effects of bilateral focal microinjection of a competitive NMDA receptor antagonist ( dl-2-amino-7-phosphonoheptanoic acid (AP7), 1 and 5 nmol/side), a GABA A agonist (gaboxedol (THIP), 10 and 15 nmol) or an opioid peptide receptor antagonist (naloxone, 5 nmol) into PAG, based on the proposed role of these receptors in PAG neurotransmission. Blockade of NMDA receptors by AP7 (both doses) or activation of GABA A receptors with THIP (15 nmol/side) in the PAG suppressed AGS susceptibility. Naloxone displayed a seizure-suppressant effect that was delayed and incomplete. The seizure suppressant effect of AP7 or naloxone, unlike THIP, was observed at doses that did not produce motor quiescence. These data suggest that the PAG is a requisite nucleus in the neuronal network for AGS in GEPR-9s and that GABA A, opioid peptide and NMDA receptors in the PAG modulate AGS propagation.
doi_str_mv 10.1016/S0920-1211(98)00128-4
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_69734927</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0920121198001284</els_id><sourcerecordid>69734927</sourcerecordid><originalsourceid>FETCH-LOGICAL-e292t-c9f05c7ffd7b22257aec684f14b96f13b06b149777a9f860d8fea1431403b07c3</originalsourceid><addsrcrecordid>eNo9kc1u1TAQRi1ERS-FRwDNCoFEwHbcOO4GhdIWpAILytpy7HEx5MbBdoour8BL4_7AaqSZo9F8cwh5wugrRln3-gtVnDaMM_Zc9S8oZbxvxD2yYb3kTdcLcZ9s_iP75GHO3ymlkgrxgOwzylsuVbshfy6-ISyYgvm5olttMRNcJtxByGDAplCCra0cCkKYoVR6xjXFuTZnLL9i-gE-JjCrC_ES52AhY_i9JsxHsI1unUwJcYZxB2fD2wGGl_Dp47sBzOwgLiEGBwktLiWm_IjseTNlfHxXD8jX05OL4_fN-eezD8fDeYNc8dJY5emhld47OXLOD6VBWwN7JkbVedaOtBuZUFJKo3zfUdd7NEy0TNA6k7Y9IM9u9y4p1tS56G3IFqfJzBjXrDslW6G4rODTO3Adt-j0ksLWpJ3-974KvLkFsJ57FTDpbAPOFl2oqYp2MVRYXwvTN8L0tQ2ten0jTIv2L-6Bh5w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>69734927</pqid></control><display><type>article</type><title>The periaqueductal grey is a critical site in the neuronal network for audiogenic seizures: modulation by GABA A, NMDA and opioid receptors</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><creator>N’Gouemo, Prosper ; Faingold, Carl L</creator><creatorcontrib>N’Gouemo, Prosper ; Faingold, Carl L</creatorcontrib><description>The nuclei comprising the neuronal network for audiogenic seizures (AGS) are located primarily in the brainstem. Previous studies suggested a role for the periaqueductal grey (PAG) in the AGS network. The present study evaluated this possibility in genetically-epilepsy prone rats (GEPR-9s) by examining the effects of bilateral focal microinjection of a competitive NMDA receptor antagonist ( dl-2-amino-7-phosphonoheptanoic acid (AP7), 1 and 5 nmol/side), a GABA A agonist (gaboxedol (THIP), 10 and 15 nmol) or an opioid peptide receptor antagonist (naloxone, 5 nmol) into PAG, based on the proposed role of these receptors in PAG neurotransmission. Blockade of NMDA receptors by AP7 (both doses) or activation of GABA A receptors with THIP (15 nmol/side) in the PAG suppressed AGS susceptibility. Naloxone displayed a seizure-suppressant effect that was delayed and incomplete. The seizure suppressant effect of AP7 or naloxone, unlike THIP, was observed at doses that did not produce motor quiescence. These data suggest that the PAG is a requisite nucleus in the neuronal network for AGS in GEPR-9s and that GABA A, opioid peptide and NMDA receptors in the PAG modulate AGS propagation.</description><identifier>ISSN: 0920-1211</identifier><identifier>EISSN: 1872-6844</identifier><identifier>DOI: 10.1016/S0920-1211(98)00128-4</identifier><identifier>PMID: 10232793</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>2-Amino-5-phosphonovalerate - analogs &amp; derivatives ; 2-Amino-5-phosphonovalerate - pharmacology ; Animals ; Audiogenic seizures ; Excitatory Amino Acid Agonists - pharmacology ; Excitatory Amino Acid Antagonists - pharmacology ; GABA ; GABA-A Receptor Agonists ; Isoxazoles - pharmacology ; Male ; Microinjections ; Naloxone ; Naloxone - pharmacology ; Narcotic Antagonists - pharmacology ; Nerve Net - pathology ; Nerve Net - physiopathology ; Neuronal network ; NMDA ; Periaqueductal Gray - pathology ; Periaqueductal Gray - physiopathology ; Periaqueductal grey ; Rats ; Receptors, GABA-A - drug effects ; Receptors, N-Methyl-D-Aspartate - antagonists &amp; inhibitors ; Receptors, N-Methyl-D-Aspartate - drug effects ; Receptors, Opioid - drug effects ; Seizures - genetics ; Seizures - physiopathology</subject><ispartof>Epilepsy research, 1999-05, Vol.35 (1), p.39-46</ispartof><rights>1999 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0920-1211(98)00128-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10232793$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>N’Gouemo, Prosper</creatorcontrib><creatorcontrib>Faingold, Carl L</creatorcontrib><title>The periaqueductal grey is a critical site in the neuronal network for audiogenic seizures: modulation by GABA A, NMDA and opioid receptors</title><title>Epilepsy research</title><addtitle>Epilepsy Res</addtitle><description>The nuclei comprising the neuronal network for audiogenic seizures (AGS) are located primarily in the brainstem. Previous studies suggested a role for the periaqueductal grey (PAG) in the AGS network. The present study evaluated this possibility in genetically-epilepsy prone rats (GEPR-9s) by examining the effects of bilateral focal microinjection of a competitive NMDA receptor antagonist ( dl-2-amino-7-phosphonoheptanoic acid (AP7), 1 and 5 nmol/side), a GABA A agonist (gaboxedol (THIP), 10 and 15 nmol) or an opioid peptide receptor antagonist (naloxone, 5 nmol) into PAG, based on the proposed role of these receptors in PAG neurotransmission. Blockade of NMDA receptors by AP7 (both doses) or activation of GABA A receptors with THIP (15 nmol/side) in the PAG suppressed AGS susceptibility. Naloxone displayed a seizure-suppressant effect that was delayed and incomplete. The seizure suppressant effect of AP7 or naloxone, unlike THIP, was observed at doses that did not produce motor quiescence. These data suggest that the PAG is a requisite nucleus in the neuronal network for AGS in GEPR-9s and that GABA A, opioid peptide and NMDA receptors in the PAG modulate AGS propagation.</description><subject>2-Amino-5-phosphonovalerate - analogs &amp; derivatives</subject><subject>2-Amino-5-phosphonovalerate - pharmacology</subject><subject>Animals</subject><subject>Audiogenic seizures</subject><subject>Excitatory Amino Acid Agonists - pharmacology</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>GABA</subject><subject>GABA-A Receptor Agonists</subject><subject>Isoxazoles - pharmacology</subject><subject>Male</subject><subject>Microinjections</subject><subject>Naloxone</subject><subject>Naloxone - pharmacology</subject><subject>Narcotic Antagonists - pharmacology</subject><subject>Nerve Net - pathology</subject><subject>Nerve Net - physiopathology</subject><subject>Neuronal network</subject><subject>NMDA</subject><subject>Periaqueductal Gray - pathology</subject><subject>Periaqueductal Gray - physiopathology</subject><subject>Periaqueductal grey</subject><subject>Rats</subject><subject>Receptors, GABA-A - drug effects</subject><subject>Receptors, N-Methyl-D-Aspartate - antagonists &amp; inhibitors</subject><subject>Receptors, N-Methyl-D-Aspartate - drug effects</subject><subject>Receptors, Opioid - drug effects</subject><subject>Seizures - genetics</subject><subject>Seizures - physiopathology</subject><issn>0920-1211</issn><issn>1872-6844</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kc1u1TAQRi1ERS-FRwDNCoFEwHbcOO4GhdIWpAILytpy7HEx5MbBdoour8BL4_7AaqSZo9F8cwh5wugrRln3-gtVnDaMM_Zc9S8oZbxvxD2yYb3kTdcLcZ9s_iP75GHO3ymlkgrxgOwzylsuVbshfy6-ISyYgvm5olttMRNcJtxByGDAplCCra0cCkKYoVR6xjXFuTZnLL9i-gE-JjCrC_ES52AhY_i9JsxHsI1unUwJcYZxB2fD2wGGl_Dp47sBzOwgLiEGBwktLiWm_IjseTNlfHxXD8jX05OL4_fN-eezD8fDeYNc8dJY5emhld47OXLOD6VBWwN7JkbVedaOtBuZUFJKo3zfUdd7NEy0TNA6k7Y9IM9u9y4p1tS56G3IFqfJzBjXrDslW6G4rODTO3Adt-j0ksLWpJ3-974KvLkFsJ57FTDpbAPOFl2oqYp2MVRYXwvTN8L0tQ2ten0jTIv2L-6Bh5w</recordid><startdate>19990501</startdate><enddate>19990501</enddate><creator>N’Gouemo, Prosper</creator><creator>Faingold, Carl L</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19990501</creationdate><title>The periaqueductal grey is a critical site in the neuronal network for audiogenic seizures: modulation by GABA A, NMDA and opioid receptors</title><author>N’Gouemo, Prosper ; Faingold, Carl L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e292t-c9f05c7ffd7b22257aec684f14b96f13b06b149777a9f860d8fea1431403b07c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>2-Amino-5-phosphonovalerate - analogs &amp; derivatives</topic><topic>2-Amino-5-phosphonovalerate - pharmacology</topic><topic>Animals</topic><topic>Audiogenic seizures</topic><topic>Excitatory Amino Acid Agonists - pharmacology</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>GABA</topic><topic>GABA-A Receptor Agonists</topic><topic>Isoxazoles - pharmacology</topic><topic>Male</topic><topic>Microinjections</topic><topic>Naloxone</topic><topic>Naloxone - pharmacology</topic><topic>Narcotic Antagonists - pharmacology</topic><topic>Nerve Net - pathology</topic><topic>Nerve Net - physiopathology</topic><topic>Neuronal network</topic><topic>NMDA</topic><topic>Periaqueductal Gray - pathology</topic><topic>Periaqueductal Gray - physiopathology</topic><topic>Periaqueductal grey</topic><topic>Rats</topic><topic>Receptors, GABA-A - drug effects</topic><topic>Receptors, N-Methyl-D-Aspartate - antagonists &amp; inhibitors</topic><topic>Receptors, N-Methyl-D-Aspartate - drug effects</topic><topic>Receptors, Opioid - drug effects</topic><topic>Seizures - genetics</topic><topic>Seizures - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>N’Gouemo, Prosper</creatorcontrib><creatorcontrib>Faingold, Carl L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Epilepsy research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>N’Gouemo, Prosper</au><au>Faingold, Carl L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The periaqueductal grey is a critical site in the neuronal network for audiogenic seizures: modulation by GABA A, NMDA and opioid receptors</atitle><jtitle>Epilepsy research</jtitle><addtitle>Epilepsy Res</addtitle><date>1999-05-01</date><risdate>1999</risdate><volume>35</volume><issue>1</issue><spage>39</spage><epage>46</epage><pages>39-46</pages><issn>0920-1211</issn><eissn>1872-6844</eissn><abstract>The nuclei comprising the neuronal network for audiogenic seizures (AGS) are located primarily in the brainstem. Previous studies suggested a role for the periaqueductal grey (PAG) in the AGS network. The present study evaluated this possibility in genetically-epilepsy prone rats (GEPR-9s) by examining the effects of bilateral focal microinjection of a competitive NMDA receptor antagonist ( dl-2-amino-7-phosphonoheptanoic acid (AP7), 1 and 5 nmol/side), a GABA A agonist (gaboxedol (THIP), 10 and 15 nmol) or an opioid peptide receptor antagonist (naloxone, 5 nmol) into PAG, based on the proposed role of these receptors in PAG neurotransmission. Blockade of NMDA receptors by AP7 (both doses) or activation of GABA A receptors with THIP (15 nmol/side) in the PAG suppressed AGS susceptibility. Naloxone displayed a seizure-suppressant effect that was delayed and incomplete. The seizure suppressant effect of AP7 or naloxone, unlike THIP, was observed at doses that did not produce motor quiescence. These data suggest that the PAG is a requisite nucleus in the neuronal network for AGS in GEPR-9s and that GABA A, opioid peptide and NMDA receptors in the PAG modulate AGS propagation.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>10232793</pmid><doi>10.1016/S0920-1211(98)00128-4</doi><tpages>8</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0920-1211
ispartof Epilepsy research, 1999-05, Vol.35 (1), p.39-46
issn 0920-1211
1872-6844
language eng
recordid cdi_proquest_miscellaneous_69734927
source MEDLINE; ScienceDirect Journals (5 years ago - present)
subjects 2-Amino-5-phosphonovalerate - analogs & derivatives
2-Amino-5-phosphonovalerate - pharmacology
Animals
Audiogenic seizures
Excitatory Amino Acid Agonists - pharmacology
Excitatory Amino Acid Antagonists - pharmacology
GABA
GABA-A Receptor Agonists
Isoxazoles - pharmacology
Male
Microinjections
Naloxone
Naloxone - pharmacology
Narcotic Antagonists - pharmacology
Nerve Net - pathology
Nerve Net - physiopathology
Neuronal network
NMDA
Periaqueductal Gray - pathology
Periaqueductal Gray - physiopathology
Periaqueductal grey
Rats
Receptors, GABA-A - drug effects
Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors
Receptors, N-Methyl-D-Aspartate - drug effects
Receptors, Opioid - drug effects
Seizures - genetics
Seizures - physiopathology
title The periaqueductal grey is a critical site in the neuronal network for audiogenic seizures: modulation by GABA A, NMDA and opioid receptors
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T16%3A13%3A49IST&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=The%20periaqueductal%20grey%20is%20a%20critical%20site%20in%20the%20neuronal%20network%20for%20audiogenic%20seizures:%20modulation%20by%20GABA%20A,%20NMDA%20and%20opioid%20receptors&rft.jtitle=Epilepsy%20research&rft.au=N%E2%80%99Gouemo,%20Prosper&rft.date=1999-05-01&rft.volume=35&rft.issue=1&rft.spage=39&rft.epage=46&rft.pages=39-46&rft.issn=0920-1211&rft.eissn=1872-6844&rft_id=info:doi/10.1016/S0920-1211(98)00128-4&rft_dat=%3Cproquest_pubme%3E69734927%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=69734927&rft_id=info:pmid/10232793&rft_els_id=S0920121198001284&rfr_iscdi=true