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Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients
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| Zeitschriftentitel: | Epilepsia |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Epilepsia, 50, 2009, 7, S. 1697-1716 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Teichgräber, Laura A. Lehmann, Thomas‐Nicolas Meencke, Heinz‐Joachim Weiss, Torsten Nitsch, Robert Deisz, Rudolf A. Teichgräber, Laura A. Lehmann, Thomas‐Nicolas Meencke, Heinz‐Joachim Weiss, Torsten Nitsch, Robert Deisz, Rudolf A. |
|---|---|
| author |
Teichgräber, Laura A. Lehmann, Thomas‐Nicolas Meencke, Heinz‐Joachim Weiss, Torsten Nitsch, Robert Deisz, Rudolf A. |
| spellingShingle |
Teichgräber, Laura A. Lehmann, Thomas‐Nicolas Meencke, Heinz‐Joachim Weiss, Torsten Nitsch, Robert Deisz, Rudolf A. Epilepsia Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients Neurology (clinical) Neurology |
| author_sort |
teichgräber, laura a. |
| spelling |
Teichgräber, Laura A. Lehmann, Thomas‐Nicolas Meencke, Heinz‐Joachim Weiss, Torsten Nitsch, Robert Deisz, Rudolf A. 0013-9580 1528-1167 Wiley Neurology (clinical) Neurology http://dx.doi.org/10.1111/j.1528-1167.2009.02094.x <jats:title>Summary</jats:title><jats:p><jats:bold><jats:styled-content>Purpose:</jats:styled-content> </jats:bold> Effects of pre‐ and postsynaptic γ‐aminobutyric acid B (GABA<jats:sub>B</jats:sub>) receptor activation were characterized in human tissue from epilepsy surgery.</jats:p><jats:p><jats:bold><jats:styled-content>Methods:</jats:styled-content> </jats:bold> Slices of human cortical tissue were investigated in a submerged‐type chamber with intracellular recordings in layers II/III. Parallel experiments were performed in rat neocortical slices with identical methods. Synaptic responses were elicited with single or paired stimulations of incrementing intervals.</jats:p><jats:p><jats:bold><jats:styled-content>Results:</jats:styled-content> </jats:bold> Neurons in human epileptogenic tissue exhibited usually small inhibitory postsynaptic potentials (IPSP) mediated by GABA<jats:sub>B</jats:sub> receptor, verified by the sensitivity to the selective antagonist CGP 55845A. The IPSP<jats:sub>B</jats:sub> conductance averaged 5.8 nS in neurons from epileptogenic tissues and 15.9 nS in neurons from nonepileptogenic tissues (p<jats:italic> </jats:italic><<jats:italic> </jats:italic>0.0001). Application of baclofen caused small conductance increases in human neurons, which were linearly related to IPSP<jats:sub>B</jats:sub> conductances. Paired‐pulse stimulation revealed constant synaptic responses in human temporal lobe epilepsy (TLE) slices at all interstimulus intervals (ISIs). Pharmacologically isolated IPSP<jats:sub>A</jats:sub> in the human tissue exhibited a small paired‐pulse depression (average 10% at 500 ms ISI). Bicuculline‐induced paroxysmal depolarization shifts (PDSs) were transiently depressed by 24% in human TLE tissue; and by 74% in rat neocortical slices (200 ms ISI; p<jats:italic> </jats:italic>=<jats:italic> </jats:italic>0.015). The depressions of bicuculline‐induced PDSs were antagonized by CGP 55845A in both species. Staining for GABA<jats:sub>B</jats:sub> receptors revealed significantly smaller numbers of immunopositive dots in human epileptogenic neurons versus human control neurons.</jats:p><jats:p><jats:bold><jats:styled-content>Discussion:</jats:styled-content> </jats:bold> The small IPSP<jats:sub>B</jats:sub>, baclofen‐conductances, and paired‐pulse depression of PDSs and IPSPs in human TLE tissue indicate a reduced density of post‐ and presynaptic GABA<jats:sub>B</jats:sub> receptors. The reduced efficacy of presynaptic GABA<jats:sub>B</jats:sub> receptors facilitates the occurrence of repetitive synaptic activity.</jats:p> Impaired function of GABA<sub>B</sub> receptors in tissues from pharmacoresistant epilepsy patients Epilepsia |
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10.1111/j.1528-1167.2009.02094.x |
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Online Free |
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Medizin |
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Wiley, 2009 |
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Wiley, 2009 |
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2009 |
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Wiley |
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Epilepsia |
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49 |
| title |
Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_unstemmed |
Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_full |
Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_fullStr |
Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_full_unstemmed |
Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_short |
Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_sort |
impaired function of gaba<sub>b</sub> receptors in tissues from pharmacoresistant epilepsy patients |
| topic |
Neurology (clinical) Neurology |
| url |
http://dx.doi.org/10.1111/j.1528-1167.2009.02094.x |
| publishDate |
2009 |
| physical |
1697-1716 |
| description |
<jats:title>Summary</jats:title><jats:p><jats:bold><jats:styled-content>Purpose:</jats:styled-content> </jats:bold> Effects of pre‐ and postsynaptic γ‐aminobutyric acid B (GABA<jats:sub>B</jats:sub>) receptor activation were characterized in human tissue from epilepsy surgery.</jats:p><jats:p><jats:bold><jats:styled-content>Methods:</jats:styled-content> </jats:bold> Slices of human cortical tissue were investigated in a submerged‐type chamber with intracellular recordings in layers II/III. Parallel experiments were performed in rat neocortical slices with identical methods. Synaptic responses were elicited with single or paired stimulations of incrementing intervals.</jats:p><jats:p><jats:bold><jats:styled-content>Results:</jats:styled-content> </jats:bold> Neurons in human epileptogenic tissue exhibited usually small inhibitory postsynaptic potentials (IPSP) mediated by GABA<jats:sub>B</jats:sub> receptor, verified by the sensitivity to the selective antagonist CGP 55845A. The IPSP<jats:sub>B</jats:sub> conductance averaged 5.8 nS in neurons from epileptogenic tissues and 15.9 nS in neurons from nonepileptogenic tissues (p<jats:italic> </jats:italic><<jats:italic> </jats:italic>0.0001). Application of baclofen caused small conductance increases in human neurons, which were linearly related to IPSP<jats:sub>B</jats:sub> conductances. Paired‐pulse stimulation revealed constant synaptic responses in human temporal lobe epilepsy (TLE) slices at all interstimulus intervals (ISIs). Pharmacologically isolated IPSP<jats:sub>A</jats:sub> in the human tissue exhibited a small paired‐pulse depression (average 10% at 500 ms ISI). Bicuculline‐induced paroxysmal depolarization shifts (PDSs) were transiently depressed by 24% in human TLE tissue; and by 74% in rat neocortical slices (200 ms ISI; p<jats:italic> </jats:italic>=<jats:italic> </jats:italic>0.015). The depressions of bicuculline‐induced PDSs were antagonized by CGP 55845A in both species. Staining for GABA<jats:sub>B</jats:sub> receptors revealed significantly smaller numbers of immunopositive dots in human epileptogenic neurons versus human control neurons.</jats:p><jats:p><jats:bold><jats:styled-content>Discussion:</jats:styled-content> </jats:bold> The small IPSP<jats:sub>B</jats:sub>, baclofen‐conductances, and paired‐pulse depression of PDSs and IPSPs in human TLE tissue indicate a reduced density of post‐ and presynaptic GABA<jats:sub>B</jats:sub> receptors. The reduced efficacy of presynaptic GABA<jats:sub>B</jats:sub> receptors facilitates the occurrence of repetitive synaptic activity.</jats:p> |
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| author | Teichgräber, Laura A., Lehmann, Thomas‐Nicolas, Meencke, Heinz‐Joachim, Weiss, Torsten, Nitsch, Robert, Deisz, Rudolf A. |
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| description | <jats:title>Summary</jats:title><jats:p><jats:bold><jats:styled-content>Purpose:</jats:styled-content> </jats:bold> Effects of pre‐ and postsynaptic γ‐aminobutyric acid B (GABA<jats:sub>B</jats:sub>) receptor activation were characterized in human tissue from epilepsy surgery.</jats:p><jats:p><jats:bold><jats:styled-content>Methods:</jats:styled-content> </jats:bold> Slices of human cortical tissue were investigated in a submerged‐type chamber with intracellular recordings in layers II/III. Parallel experiments were performed in rat neocortical slices with identical methods. Synaptic responses were elicited with single or paired stimulations of incrementing intervals.</jats:p><jats:p><jats:bold><jats:styled-content>Results:</jats:styled-content> </jats:bold> Neurons in human epileptogenic tissue exhibited usually small inhibitory postsynaptic potentials (IPSP) mediated by GABA<jats:sub>B</jats:sub> receptor, verified by the sensitivity to the selective antagonist CGP 55845A. The IPSP<jats:sub>B</jats:sub> conductance averaged 5.8 nS in neurons from epileptogenic tissues and 15.9 nS in neurons from nonepileptogenic tissues (p<jats:italic> </jats:italic><<jats:italic> </jats:italic>0.0001). Application of baclofen caused small conductance increases in human neurons, which were linearly related to IPSP<jats:sub>B</jats:sub> conductances. Paired‐pulse stimulation revealed constant synaptic responses in human temporal lobe epilepsy (TLE) slices at all interstimulus intervals (ISIs). Pharmacologically isolated IPSP<jats:sub>A</jats:sub> in the human tissue exhibited a small paired‐pulse depression (average 10% at 500 ms ISI). Bicuculline‐induced paroxysmal depolarization shifts (PDSs) were transiently depressed by 24% in human TLE tissue; and by 74% in rat neocortical slices (200 ms ISI; p<jats:italic> </jats:italic>=<jats:italic> </jats:italic>0.015). The depressions of bicuculline‐induced PDSs were antagonized by CGP 55845A in both species. Staining for GABA<jats:sub>B</jats:sub> receptors revealed significantly smaller numbers of immunopositive dots in human epileptogenic neurons versus human control neurons.</jats:p><jats:p><jats:bold><jats:styled-content>Discussion:</jats:styled-content> </jats:bold> The small IPSP<jats:sub>B</jats:sub>, baclofen‐conductances, and paired‐pulse depression of PDSs and IPSPs in human TLE tissue indicate a reduced density of post‐ and presynaptic GABA<jats:sub>B</jats:sub> receptors. The reduced efficacy of presynaptic GABA<jats:sub>B</jats:sub> receptors facilitates the occurrence of repetitive synaptic activity.</jats:p> |
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| spelling | Teichgräber, Laura A. Lehmann, Thomas‐Nicolas Meencke, Heinz‐Joachim Weiss, Torsten Nitsch, Robert Deisz, Rudolf A. 0013-9580 1528-1167 Wiley Neurology (clinical) Neurology http://dx.doi.org/10.1111/j.1528-1167.2009.02094.x <jats:title>Summary</jats:title><jats:p><jats:bold><jats:styled-content>Purpose:</jats:styled-content> </jats:bold> Effects of pre‐ and postsynaptic γ‐aminobutyric acid B (GABA<jats:sub>B</jats:sub>) receptor activation were characterized in human tissue from epilepsy surgery.</jats:p><jats:p><jats:bold><jats:styled-content>Methods:</jats:styled-content> </jats:bold> Slices of human cortical tissue were investigated in a submerged‐type chamber with intracellular recordings in layers II/III. Parallel experiments were performed in rat neocortical slices with identical methods. Synaptic responses were elicited with single or paired stimulations of incrementing intervals.</jats:p><jats:p><jats:bold><jats:styled-content>Results:</jats:styled-content> </jats:bold> Neurons in human epileptogenic tissue exhibited usually small inhibitory postsynaptic potentials (IPSP) mediated by GABA<jats:sub>B</jats:sub> receptor, verified by the sensitivity to the selective antagonist CGP 55845A. The IPSP<jats:sub>B</jats:sub> conductance averaged 5.8 nS in neurons from epileptogenic tissues and 15.9 nS in neurons from nonepileptogenic tissues (p<jats:italic> </jats:italic><<jats:italic> </jats:italic>0.0001). Application of baclofen caused small conductance increases in human neurons, which were linearly related to IPSP<jats:sub>B</jats:sub> conductances. Paired‐pulse stimulation revealed constant synaptic responses in human temporal lobe epilepsy (TLE) slices at all interstimulus intervals (ISIs). Pharmacologically isolated IPSP<jats:sub>A</jats:sub> in the human tissue exhibited a small paired‐pulse depression (average 10% at 500 ms ISI). Bicuculline‐induced paroxysmal depolarization shifts (PDSs) were transiently depressed by 24% in human TLE tissue; and by 74% in rat neocortical slices (200 ms ISI; p<jats:italic> </jats:italic>=<jats:italic> </jats:italic>0.015). The depressions of bicuculline‐induced PDSs were antagonized by CGP 55845A in both species. Staining for GABA<jats:sub>B</jats:sub> receptors revealed significantly smaller numbers of immunopositive dots in human epileptogenic neurons versus human control neurons.</jats:p><jats:p><jats:bold><jats:styled-content>Discussion:</jats:styled-content> </jats:bold> The small IPSP<jats:sub>B</jats:sub>, baclofen‐conductances, and paired‐pulse depression of PDSs and IPSPs in human TLE tissue indicate a reduced density of post‐ and presynaptic GABA<jats:sub>B</jats:sub> receptors. The reduced efficacy of presynaptic GABA<jats:sub>B</jats:sub> receptors facilitates the occurrence of repetitive synaptic activity.</jats:p> Impaired function of GABA<sub>B</sub> receptors in tissues from pharmacoresistant epilepsy patients Epilepsia |
| spellingShingle | Teichgräber, Laura A., Lehmann, Thomas‐Nicolas, Meencke, Heinz‐Joachim, Weiss, Torsten, Nitsch, Robert, Deisz, Rudolf A., Epilepsia, Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients, Neurology (clinical), Neurology |
| title | Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_full | Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_fullStr | Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_full_unstemmed | Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_short | Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| title_sort | impaired function of gaba<sub>b</sub> receptors in tissues from pharmacoresistant epilepsy patients |
| title_unstemmed | Impaired function of GABAB receptors in tissues from pharmacoresistant epilepsy patients |
| topic | Neurology (clinical), Neurology |
| url | http://dx.doi.org/10.1111/j.1528-1167.2009.02094.x |