Long-term potentiation of primary afferent neurotransmission at trigeminal synapses of juvenile rats
Primary afferent monosynaptic and polysynaptic excitatory postsynaptic currents (EPSCs) were recorded from brainstem trigeminal neurons by stimulation of the mandibular nerve attached to the brainstem preparation of juvenile rats. A high-frequency conditioning stimulus induced long-term potentiation...
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| Autor*in: |
Hamba, Michiko [verfasserIn] Onodera, Kayoko [verfasserIn] Takahashi, Tomoyuki [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2000 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2001 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: European journal of neuroscience - Oxford [u.a.] : Blackwell, 1989, 12(2000), 3, Seite 0 |
| Übergeordnetes Werk: |
volume:12 ; year:2000 ; number:3 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1046/j.1460-9568.2000.01028.x |
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| 520 | |a Primary afferent monosynaptic and polysynaptic excitatory postsynaptic currents (EPSCs) were recorded from brainstem trigeminal neurons by stimulation of the mandibular nerve attached to the brainstem preparation of juvenile rats. A high-frequency conditioning stimulus induced long-term potentiation (LTP) of high-threshold EPSCs in the majority of trigeminal caudal neurons in substantia gelatinosa, where both A- and C-fibres terminate. However, the same conditioning stimulus did not potentiate low-threshold EPSCs in caudal neurons or EPSCs recorded from neurons in the middle part of trigeminal interpolar nucleus, where C-fibres rarely terminate. LTP in caudal neurons could be induced after blocking N-methyl- d-aspartate (NMDA) receptors with D(–)-2-amino-5-phosphonopentanoic acid (D-AP5, 50 μm), after postsynaptic loading of the Ca2+ chelator BAPTA (10 m m), or even after completely blocking excitatory transmission with kynurenic acid during conditioning. However, LTP was blocked by the metabotropic glutamate receptor antagonist (+)-α-methyl-4-carboxyphenylglycine (1 m m). We suggest that LTP of the trigeminal primary afferent EPSCs is induced preferentially in the C-fibre inputs and that the induction mechanism involves metabotropic glutamate receptors, possibly at the presynaptic terminals. | ||
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10.1046/j.1460-9568.2000.01028.x doi (DE-627)NLEJ242441165 DE-627 ger DE-627 rakwb Hamba, Michiko verfasserin aut Long-term potentiation of primary afferent neurotransmission at trigeminal synapses of juvenile rats Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Primary afferent monosynaptic and polysynaptic excitatory postsynaptic currents (EPSCs) were recorded from brainstem trigeminal neurons by stimulation of the mandibular nerve attached to the brainstem preparation of juvenile rats. A high-frequency conditioning stimulus induced long-term potentiation (LTP) of high-threshold EPSCs in the majority of trigeminal caudal neurons in substantia gelatinosa, where both A- and C-fibres terminate. However, the same conditioning stimulus did not potentiate low-threshold EPSCs in caudal neurons or EPSCs recorded from neurons in the middle part of trigeminal interpolar nucleus, where C-fibres rarely terminate. LTP in caudal neurons could be induced after blocking N-methyl- d-aspartate (NMDA) receptors with D(–)-2-amino-5-phosphonopentanoic acid (D-AP5, 50 μm), after postsynaptic loading of the Ca2+ chelator BAPTA (10 m m), or even after completely blocking excitatory transmission with kynurenic acid during conditioning. However, LTP was blocked by the metabotropic glutamate receptor antagonist (+)-α-methyl-4-carboxyphenylglycine (1 m m). We suggest that LTP of the trigeminal primary afferent EPSCs is induced preferentially in the C-fibre inputs and that the induction mechanism involves metabotropic glutamate receptors, possibly at the presynaptic terminals. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| LTP Onodera, Kayoko verfasserin aut Takahashi, Tomoyuki verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 12(2000), 3, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:12 year:2000 number:3 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2000.01028.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 12 2000 3 0 |
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10.1046/j.1460-9568.2000.01028.x doi (DE-627)NLEJ242441165 DE-627 ger DE-627 rakwb Hamba, Michiko verfasserin aut Long-term potentiation of primary afferent neurotransmission at trigeminal synapses of juvenile rats Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Primary afferent monosynaptic and polysynaptic excitatory postsynaptic currents (EPSCs) were recorded from brainstem trigeminal neurons by stimulation of the mandibular nerve attached to the brainstem preparation of juvenile rats. A high-frequency conditioning stimulus induced long-term potentiation (LTP) of high-threshold EPSCs in the majority of trigeminal caudal neurons in substantia gelatinosa, where both A- and C-fibres terminate. However, the same conditioning stimulus did not potentiate low-threshold EPSCs in caudal neurons or EPSCs recorded from neurons in the middle part of trigeminal interpolar nucleus, where C-fibres rarely terminate. LTP in caudal neurons could be induced after blocking N-methyl- d-aspartate (NMDA) receptors with D(–)-2-amino-5-phosphonopentanoic acid (D-AP5, 50 μm), after postsynaptic loading of the Ca2+ chelator BAPTA (10 m m), or even after completely blocking excitatory transmission with kynurenic acid during conditioning. However, LTP was blocked by the metabotropic glutamate receptor antagonist (+)-α-methyl-4-carboxyphenylglycine (1 m m). We suggest that LTP of the trigeminal primary afferent EPSCs is induced preferentially in the C-fibre inputs and that the induction mechanism involves metabotropic glutamate receptors, possibly at the presynaptic terminals. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| LTP Onodera, Kayoko verfasserin aut Takahashi, Tomoyuki verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 12(2000), 3, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:12 year:2000 number:3 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2000.01028.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 12 2000 3 0 |
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10.1046/j.1460-9568.2000.01028.x doi (DE-627)NLEJ242441165 DE-627 ger DE-627 rakwb Hamba, Michiko verfasserin aut Long-term potentiation of primary afferent neurotransmission at trigeminal synapses of juvenile rats Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Primary afferent monosynaptic and polysynaptic excitatory postsynaptic currents (EPSCs) were recorded from brainstem trigeminal neurons by stimulation of the mandibular nerve attached to the brainstem preparation of juvenile rats. A high-frequency conditioning stimulus induced long-term potentiation (LTP) of high-threshold EPSCs in the majority of trigeminal caudal neurons in substantia gelatinosa, where both A- and C-fibres terminate. However, the same conditioning stimulus did not potentiate low-threshold EPSCs in caudal neurons or EPSCs recorded from neurons in the middle part of trigeminal interpolar nucleus, where C-fibres rarely terminate. LTP in caudal neurons could be induced after blocking N-methyl- d-aspartate (NMDA) receptors with D(–)-2-amino-5-phosphonopentanoic acid (D-AP5, 50 μm), after postsynaptic loading of the Ca2+ chelator BAPTA (10 m m), or even after completely blocking excitatory transmission with kynurenic acid during conditioning. However, LTP was blocked by the metabotropic glutamate receptor antagonist (+)-α-methyl-4-carboxyphenylglycine (1 m m). We suggest that LTP of the trigeminal primary afferent EPSCs is induced preferentially in the C-fibre inputs and that the induction mechanism involves metabotropic glutamate receptors, possibly at the presynaptic terminals. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| LTP Onodera, Kayoko verfasserin aut Takahashi, Tomoyuki verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 12(2000), 3, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:12 year:2000 number:3 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2000.01028.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 12 2000 3 0 |
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10.1046/j.1460-9568.2000.01028.x doi (DE-627)NLEJ242441165 DE-627 ger DE-627 rakwb Hamba, Michiko verfasserin aut Long-term potentiation of primary afferent neurotransmission at trigeminal synapses of juvenile rats Oxford, UK Blackwell Science Ltd 2000 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Primary afferent monosynaptic and polysynaptic excitatory postsynaptic currents (EPSCs) were recorded from brainstem trigeminal neurons by stimulation of the mandibular nerve attached to the brainstem preparation of juvenile rats. A high-frequency conditioning stimulus induced long-term potentiation (LTP) of high-threshold EPSCs in the majority of trigeminal caudal neurons in substantia gelatinosa, where both A- and C-fibres terminate. However, the same conditioning stimulus did not potentiate low-threshold EPSCs in caudal neurons or EPSCs recorded from neurons in the middle part of trigeminal interpolar nucleus, where C-fibres rarely terminate. LTP in caudal neurons could be induced after blocking N-methyl- d-aspartate (NMDA) receptors with D(–)-2-amino-5-phosphonopentanoic acid (D-AP5, 50 μm), after postsynaptic loading of the Ca2+ chelator BAPTA (10 m m), or even after completely blocking excitatory transmission with kynurenic acid during conditioning. However, LTP was blocked by the metabotropic glutamate receptor antagonist (+)-α-methyl-4-carboxyphenylglycine (1 m m). We suggest that LTP of the trigeminal primary afferent EPSCs is induced preferentially in the C-fibre inputs and that the induction mechanism involves metabotropic glutamate receptors, possibly at the presynaptic terminals. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| LTP Onodera, Kayoko verfasserin aut Takahashi, Tomoyuki verfasserin aut In European journal of neuroscience Oxford [u.a.] : Blackwell, 1989 12(2000), 3, Seite 0 Online-Ressource (DE-627)NLEJ243926383 (DE-600)2005178-5 1460-9568 nnns volume:12 year:2000 number:3 pages:0 http://dx.doi.org/10.1046/j.1460-9568.2000.01028.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 12 2000 3 0 |
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Long-term potentiation of primary afferent neurotransmission at trigeminal synapses of juvenile rats |
| abstract |
Primary afferent monosynaptic and polysynaptic excitatory postsynaptic currents (EPSCs) were recorded from brainstem trigeminal neurons by stimulation of the mandibular nerve attached to the brainstem preparation of juvenile rats. A high-frequency conditioning stimulus induced long-term potentiation (LTP) of high-threshold EPSCs in the majority of trigeminal caudal neurons in substantia gelatinosa, where both A- and C-fibres terminate. However, the same conditioning stimulus did not potentiate low-threshold EPSCs in caudal neurons or EPSCs recorded from neurons in the middle part of trigeminal interpolar nucleus, where C-fibres rarely terminate. LTP in caudal neurons could be induced after blocking N-methyl- d-aspartate (NMDA) receptors with D(–)-2-amino-5-phosphonopentanoic acid (D-AP5, 50 μm), after postsynaptic loading of the Ca2+ chelator BAPTA (10 m m), or even after completely blocking excitatory transmission with kynurenic acid during conditioning. However, LTP was blocked by the metabotropic glutamate receptor antagonist (+)-α-methyl-4-carboxyphenylglycine (1 m m). We suggest that LTP of the trigeminal primary afferent EPSCs is induced preferentially in the C-fibre inputs and that the induction mechanism involves metabotropic glutamate receptors, possibly at the presynaptic terminals. |
| abstractGer |
Primary afferent monosynaptic and polysynaptic excitatory postsynaptic currents (EPSCs) were recorded from brainstem trigeminal neurons by stimulation of the mandibular nerve attached to the brainstem preparation of juvenile rats. A high-frequency conditioning stimulus induced long-term potentiation (LTP) of high-threshold EPSCs in the majority of trigeminal caudal neurons in substantia gelatinosa, where both A- and C-fibres terminate. However, the same conditioning stimulus did not potentiate low-threshold EPSCs in caudal neurons or EPSCs recorded from neurons in the middle part of trigeminal interpolar nucleus, where C-fibres rarely terminate. LTP in caudal neurons could be induced after blocking N-methyl- d-aspartate (NMDA) receptors with D(–)-2-amino-5-phosphonopentanoic acid (D-AP5, 50 μm), after postsynaptic loading of the Ca2+ chelator BAPTA (10 m m), or even after completely blocking excitatory transmission with kynurenic acid during conditioning. However, LTP was blocked by the metabotropic glutamate receptor antagonist (+)-α-methyl-4-carboxyphenylglycine (1 m m). We suggest that LTP of the trigeminal primary afferent EPSCs is induced preferentially in the C-fibre inputs and that the induction mechanism involves metabotropic glutamate receptors, possibly at the presynaptic terminals. |
| abstract_unstemmed |
Primary afferent monosynaptic and polysynaptic excitatory postsynaptic currents (EPSCs) were recorded from brainstem trigeminal neurons by stimulation of the mandibular nerve attached to the brainstem preparation of juvenile rats. A high-frequency conditioning stimulus induced long-term potentiation (LTP) of high-threshold EPSCs in the majority of trigeminal caudal neurons in substantia gelatinosa, where both A- and C-fibres terminate. However, the same conditioning stimulus did not potentiate low-threshold EPSCs in caudal neurons or EPSCs recorded from neurons in the middle part of trigeminal interpolar nucleus, where C-fibres rarely terminate. LTP in caudal neurons could be induced after blocking N-methyl- d-aspartate (NMDA) receptors with D(–)-2-amino-5-phosphonopentanoic acid (D-AP5, 50 μm), after postsynaptic loading of the Ca2+ chelator BAPTA (10 m m), or even after completely blocking excitatory transmission with kynurenic acid during conditioning. However, LTP was blocked by the metabotropic glutamate receptor antagonist (+)-α-methyl-4-carboxyphenylglycine (1 m m). We suggest that LTP of the trigeminal primary afferent EPSCs is induced preferentially in the C-fibre inputs and that the induction mechanism involves metabotropic glutamate receptors, possibly at the presynaptic terminals. |
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Long-term potentiation of primary afferent neurotransmission at trigeminal synapses of juvenile rats |
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Onodera, Kayoko Takahashi, Tomoyuki |
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