Changes in inhibitory neurotransmission in the CA1 region and dentate gyrus in a chronic model of temporal lobe epilepsy
P. S. Mangan, D. A. Rempe and E. W. Lothman Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908, USA. 1. In this report we compare changes in inhibitory neurotransmission within the CA1 region and the dentate gyrus (DG) in a model of chronic temporal lobe ep...
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| Veröffentlicht in: | Journal of neurophysiology 1995-08, Vol.74 (2), p.829-840 |
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| creator | Mangan, P. S Rempe, D. A Lothman, E. W |
| description | P. S. Mangan, D. A. Rempe and E. W. Lothman
Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
1. In this report we compare changes in inhibitory neurotransmission within
the CA1 region and the dentate gyrus (DG) in a model of chronic temporal
lobe epilepsy (TLE). Extracellular and intracellular recordings were
obtained in combined hippocampal-parahippocampal slices > or = 1 mo
after a period of self-sustaining limbic status epilepticus (SSLSE) induced
by continuous hippocampal stimulation. 2. Polysynaptic inhibitory
postsynaptic potentials (IPSPs) were induced by positioning electrodes to
activate specific afferent pathways and evoking responses in the absence of
glutamate receptor antagonists [D(-)-2-amino-5-phosphonovaleric acid (APV)
and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)]. Polysynaptic IPSPs were
evoked in CA1 pyramidal cells from electrodes positioned in stratum
radiatum and in stratum lacunosum/moleculare. Polysynaptic IPSPs were
evoked in DG granule cells from electrodes positioned over the perforant
path located in the subiculum. Monosynaptic IPSPs were induced by
positioning electrodes within 200 microns of the intracellular recording
electrode (near site stimulation) and stimulating in the presence of APV
and CNQX to block ionotropic glutamate receptors. Monosynaptic IPSPs were
evoked in CA1 pyramidal cells with electrodes positioned in the stratum
lacunosum/moleculare and stratum pyramidale. Monosynaptic IPSPs were evoked
in DG granule cells with electrodes positioned in the stratum moleculare.
3. Population spike (PS) amplitudes were employed to assure that a full
range of stimulus strengths, from subthreshold for action potentials to an
intensity giving maximal-amplitude PSs, was used to elicit polysynaptic
IPSPs in CA1 pyramidal cells in both post-SSLSE and control slices. In
control tissue, polysynaptic IPSPs were biphasic, composed of early and
late events. In post-SSLSE tissue, polysynaptic IPSPs were markedly
diminished. The diminution of polysynaptic IPSPs was detected at all levels
of stimulus intensity. Both early IPSPs [mediated by gamma-aminobutyric
acid-A (GABAA) receptors] and late IPSPs (mediated by GABAB receptors) were
diminished. Polysynaptic IPSPs were diminished with both stratum radiatum
and with stratum lacunosum/moleculare stimulation. 4. Reversal potentials
for either polysynaptic early or polysynaptic late IPSPs evoked in CA1
pyramidal cells by stratum radiatum s |
| doi_str_mv | 10.1152/jn.1995.74.2.829 |
| format | Article |
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Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
1. In this report we compare changes in inhibitory neurotransmission within
the CA1 region and the dentate gyrus (DG) in a model of chronic temporal
lobe epilepsy (TLE). Extracellular and intracellular recordings were
obtained in combined hippocampal-parahippocampal slices > or = 1 mo
after a period of self-sustaining limbic status epilepticus (SSLSE) induced
by continuous hippocampal stimulation. 2. Polysynaptic inhibitory
postsynaptic potentials (IPSPs) were induced by positioning electrodes to
activate specific afferent pathways and evoking responses in the absence of
glutamate receptor antagonists [D(-)-2-amino-5-phosphonovaleric acid (APV)
and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)]. Polysynaptic IPSPs were
evoked in CA1 pyramidal cells from electrodes positioned in stratum
radiatum and in stratum lacunosum/moleculare. Polysynaptic IPSPs were
evoked in DG granule cells from electrodes positioned over the perforant
path located in the subiculum. Monosynaptic IPSPs were induced by
positioning electrodes within 200 microns of the intracellular recording
electrode (near site stimulation) and stimulating in the presence of APV
and CNQX to block ionotropic glutamate receptors. Monosynaptic IPSPs were
evoked in CA1 pyramidal cells with electrodes positioned in the stratum
lacunosum/moleculare and stratum pyramidale. Monosynaptic IPSPs were evoked
in DG granule cells with electrodes positioned in the stratum moleculare.
3. Population spike (PS) amplitudes were employed to assure that a full
range of stimulus strengths, from subthreshold for action potentials to an
intensity giving maximal-amplitude PSs, was used to elicit polysynaptic
IPSPs in CA1 pyramidal cells in both post-SSLSE and control slices. In
control tissue, polysynaptic IPSPs were biphasic, composed of early and
late events. In post-SSLSE tissue, polysynaptic IPSPs were markedly
diminished. The diminution of polysynaptic IPSPs was detected at all levels
of stimulus intensity. Both early IPSPs [mediated by gamma-aminobutyric
acid-A (GABAA) receptors] and late IPSPs (mediated by GABAB receptors) were
diminished. Polysynaptic IPSPs were diminished with both stratum radiatum
and with stratum lacunosum/moleculare stimulation. 4. Reversal potentials
for either polysynaptic early or polysynaptic late IPSPs evoked in CA1
pyramidal cells by stratum radiatum stimulation were not different in
slices from post-SSLSE animals as compared with control animals. Likewise,
reversal potentials for either polysynaptic early or polysynaptic late
IPSPs evoked by stratum lacunosum/moleculare stimulation did not differ in
the two groups. These findings excluded changes in driving force as an
explanation for the diminished amplitude of IPSPs in CA1 pyramidal cells in
the post-SSLSE model.</description><identifier>ISSN: 0022-3077</identifier><identifier>EISSN: 1522-1598</identifier><identifier>DOI: 10.1152/jn.1995.74.2.829</identifier><identifier>PMID: 7472386</identifier><language>eng</language><publisher>United States: Am Phys Soc</publisher><subject>Animals ; Dentate Gyrus - physiopathology ; Disease Models, Animal ; Electric Stimulation ; Electrophysiology ; Epilepsy, Temporal Lobe - physiopathology ; Hippocampus - physiopathology ; Male ; Membrane Potentials ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission ; Time Factors</subject><ispartof>Journal of neurophysiology, 1995-08, Vol.74 (2), p.829-840</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c325t-fa3906d882881b201edb256d0b135b411e11f0776fe9fea7a0e75cc964a460ea3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7472386$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mangan, P. S</creatorcontrib><creatorcontrib>Rempe, D. A</creatorcontrib><creatorcontrib>Lothman, E. W</creatorcontrib><title>Changes in inhibitory neurotransmission in the CA1 region and dentate gyrus in a chronic model of temporal lobe epilepsy</title><title>Journal of neurophysiology</title><addtitle>J Neurophysiol</addtitle><description>P. S. Mangan, D. A. Rempe and E. W. Lothman
Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
1. In this report we compare changes in inhibitory neurotransmission within
the CA1 region and the dentate gyrus (DG) in a model of chronic temporal
lobe epilepsy (TLE). Extracellular and intracellular recordings were
obtained in combined hippocampal-parahippocampal slices > or = 1 mo
after a period of self-sustaining limbic status epilepticus (SSLSE) induced
by continuous hippocampal stimulation. 2. Polysynaptic inhibitory
postsynaptic potentials (IPSPs) were induced by positioning electrodes to
activate specific afferent pathways and evoking responses in the absence of
glutamate receptor antagonists [D(-)-2-amino-5-phosphonovaleric acid (APV)
and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)]. Polysynaptic IPSPs were
evoked in CA1 pyramidal cells from electrodes positioned in stratum
radiatum and in stratum lacunosum/moleculare. Polysynaptic IPSPs were
evoked in DG granule cells from electrodes positioned over the perforant
path located in the subiculum. Monosynaptic IPSPs were induced by
positioning electrodes within 200 microns of the intracellular recording
electrode (near site stimulation) and stimulating in the presence of APV
and CNQX to block ionotropic glutamate receptors. Monosynaptic IPSPs were
evoked in CA1 pyramidal cells with electrodes positioned in the stratum
lacunosum/moleculare and stratum pyramidale. Monosynaptic IPSPs were evoked
in DG granule cells with electrodes positioned in the stratum moleculare.
3. Population spike (PS) amplitudes were employed to assure that a full
range of stimulus strengths, from subthreshold for action potentials to an
intensity giving maximal-amplitude PSs, was used to elicit polysynaptic
IPSPs in CA1 pyramidal cells in both post-SSLSE and control slices. In
control tissue, polysynaptic IPSPs were biphasic, composed of early and
late events. In post-SSLSE tissue, polysynaptic IPSPs were markedly
diminished. The diminution of polysynaptic IPSPs was detected at all levels
of stimulus intensity. Both early IPSPs [mediated by gamma-aminobutyric
acid-A (GABAA) receptors] and late IPSPs (mediated by GABAB receptors) were
diminished. Polysynaptic IPSPs were diminished with both stratum radiatum
and with stratum lacunosum/moleculare stimulation. 4. Reversal potentials
for either polysynaptic early or polysynaptic late IPSPs evoked in CA1
pyramidal cells by stratum radiatum stimulation were not different in
slices from post-SSLSE animals as compared with control animals. Likewise,
reversal potentials for either polysynaptic early or polysynaptic late
IPSPs evoked by stratum lacunosum/moleculare stimulation did not differ in
the two groups. These findings excluded changes in driving force as an
explanation for the diminished amplitude of IPSPs in CA1 pyramidal cells in
the post-SSLSE model.</description><subject>Animals</subject><subject>Dentate Gyrus - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Electric Stimulation</subject><subject>Electrophysiology</subject><subject>Epilepsy, Temporal Lobe - physiopathology</subject><subject>Hippocampus - physiopathology</subject><subject>Male</subject><subject>Membrane Potentials</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Synaptic Transmission</subject><subject>Time Factors</subject><issn>0022-3077</issn><issn>1522-1598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtLxDAQgIMouj7uXoScvG1N0qZpj8viCxa86Dmk7bTN0iY1adH-e1N3UQhMmMc3zIfQLSURpZw97E1E85xHIolYlLH8BK1Cmq0pz7NTtCIk_GMixAW69H5PCBGcsHN0LhLB4ixdoe9tq0wDHmsTXqsLPVo3YwOTs6NTxvfae22XIh5bwNsNxQ6aJaNMhSswoxoBN7ObfhkKl62zRpe4txV02NZ4hH6wTnW4swVgGHQHg5-v0VmtOg83x3iFPp4e37cv693b8-t2s1uXMePjulZxTtIqy1iW0YIRClXBeFqRgsa8SCgFSutwYFpDXoMSioDgZZmniUpSAiq-QvcH7uDs5wR-lOGiErpOGbCTl0JwkfM0CY3k0Fg6672DWg5O98rNkhK5yJZ7IxfZUiSSySA7jNwd2VPRQ_U3cLT7v7vVTfulHcihnYPNzjbzQvsD_QBfkIn3</recordid><startdate>19950801</startdate><enddate>19950801</enddate><creator>Mangan, P. S</creator><creator>Rempe, D. A</creator><creator>Lothman, E. W</creator><general>Am Phys Soc</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></search><sort><creationdate>19950801</creationdate><title>Changes in inhibitory neurotransmission in the CA1 region and dentate gyrus in a chronic model of temporal lobe epilepsy</title><author>Mangan, P. S ; Rempe, D. A ; Lothman, E. W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c325t-fa3906d882881b201edb256d0b135b411e11f0776fe9fea7a0e75cc964a460ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>Dentate Gyrus - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Electric Stimulation</topic><topic>Electrophysiology</topic><topic>Epilepsy, Temporal Lobe - physiopathology</topic><topic>Hippocampus - physiopathology</topic><topic>Male</topic><topic>Membrane Potentials</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Synaptic Transmission</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mangan, P. S</creatorcontrib><creatorcontrib>Rempe, D. A</creatorcontrib><creatorcontrib>Lothman, E. W</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><jtitle>Journal of neurophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mangan, P. S</au><au>Rempe, D. A</au><au>Lothman, E. W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in inhibitory neurotransmission in the CA1 region and dentate gyrus in a chronic model of temporal lobe epilepsy</atitle><jtitle>Journal of neurophysiology</jtitle><addtitle>J Neurophysiol</addtitle><date>1995-08-01</date><risdate>1995</risdate><volume>74</volume><issue>2</issue><spage>829</spage><epage>840</epage><pages>829-840</pages><issn>0022-3077</issn><eissn>1522-1598</eissn><abstract>P. S. Mangan, D. A. Rempe and E. W. Lothman
Department of Neurology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
1. In this report we compare changes in inhibitory neurotransmission within
the CA1 region and the dentate gyrus (DG) in a model of chronic temporal
lobe epilepsy (TLE). Extracellular and intracellular recordings were
obtained in combined hippocampal-parahippocampal slices > or = 1 mo
after a period of self-sustaining limbic status epilepticus (SSLSE) induced
by continuous hippocampal stimulation. 2. Polysynaptic inhibitory
postsynaptic potentials (IPSPs) were induced by positioning electrodes to
activate specific afferent pathways and evoking responses in the absence of
glutamate receptor antagonists [D(-)-2-amino-5-phosphonovaleric acid (APV)
and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)]. Polysynaptic IPSPs were
evoked in CA1 pyramidal cells from electrodes positioned in stratum
radiatum and in stratum lacunosum/moleculare. Polysynaptic IPSPs were
evoked in DG granule cells from electrodes positioned over the perforant
path located in the subiculum. Monosynaptic IPSPs were induced by
positioning electrodes within 200 microns of the intracellular recording
electrode (near site stimulation) and stimulating in the presence of APV
and CNQX to block ionotropic glutamate receptors. Monosynaptic IPSPs were
evoked in CA1 pyramidal cells with electrodes positioned in the stratum
lacunosum/moleculare and stratum pyramidale. Monosynaptic IPSPs were evoked
in DG granule cells with electrodes positioned in the stratum moleculare.
3. Population spike (PS) amplitudes were employed to assure that a full
range of stimulus strengths, from subthreshold for action potentials to an
intensity giving maximal-amplitude PSs, was used to elicit polysynaptic
IPSPs in CA1 pyramidal cells in both post-SSLSE and control slices. In
control tissue, polysynaptic IPSPs were biphasic, composed of early and
late events. In post-SSLSE tissue, polysynaptic IPSPs were markedly
diminished. The diminution of polysynaptic IPSPs was detected at all levels
of stimulus intensity. Both early IPSPs [mediated by gamma-aminobutyric
acid-A (GABAA) receptors] and late IPSPs (mediated by GABAB receptors) were
diminished. Polysynaptic IPSPs were diminished with both stratum radiatum
and with stratum lacunosum/moleculare stimulation. 4. Reversal potentials
for either polysynaptic early or polysynaptic late IPSPs evoked in CA1
pyramidal cells by stratum radiatum stimulation were not different in
slices from post-SSLSE animals as compared with control animals. Likewise,
reversal potentials for either polysynaptic early or polysynaptic late
IPSPs evoked by stratum lacunosum/moleculare stimulation did not differ in
the two groups. These findings excluded changes in driving force as an
explanation for the diminished amplitude of IPSPs in CA1 pyramidal cells in
the post-SSLSE model.</abstract><cop>United States</cop><pub>Am Phys Soc</pub><pmid>7472386</pmid><doi>10.1152/jn.1995.74.2.829</doi><tpages>12</tpages></addata></record> |
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| ispartof | Journal of neurophysiology, 1995-08, Vol.74 (2), p.829-840 |
| issn | 0022-3077 1522-1598 |
| language | eng |
| recordid | cdi_pubmed_primary_7472386 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Dentate Gyrus - physiopathology Disease Models, Animal Electric Stimulation Electrophysiology Epilepsy, Temporal Lobe - physiopathology Hippocampus - physiopathology Male Membrane Potentials Rats Rats, Sprague-Dawley Synaptic Transmission Time Factors |
| title | Changes in inhibitory neurotransmission in the CA1 region and dentate gyrus in a chronic model of temporal lobe epilepsy |
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