Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization

Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL...
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Autor*in:	Gustafson-Vickers, Sabrina L [verfasserIn] Lu, Van B Lai, Aaron Y Todd, Kathryn G Ballanyi, Klaus Smith, Peter A

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2008

Schlagwörter:	Dorsal Horn Central Sensitization Chronic Constriction Injury Spare Nerve Injury Delay Cell

Anmerkung:	© Gustafson-Vickers et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: Molecular pain - London : Sage, 2005, 4(2008), 1 vom: 17. Dez.
Übergeordnetes Werk:	volume:4 ; year:2008 ; number:1 ; day:17 ; month:12

Links:	Volltext

DOI / URN:	10.1186/1744-8069-4-63

Katalog-ID:	SPR029304334

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520			\|a Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1β for 6–8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and $ Ca^{2+} $ imaging techniques. Results Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1β increased the change in intracellular $ Ca^{2+} $ produced by exposure to 35–50 mM $ K^{+} $. This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1β did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1β were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1β included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons. Conclusion Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1β at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1β may contribute to the central sensitization associated with chronic neuropathic pain.
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allfields	10.1186/1744-8069-4-63 doi (DE-627)SPR029304334 (SPR)1744-8069-4-63-e DE-627 ger DE-627 rakwb eng Gustafson-Vickers, Sabrina L verfasserin aut Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gustafson-Vickers et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1β for 6–8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and $ Ca^{2+} $ imaging techniques. Results Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1β increased the change in intracellular $ Ca^{2+} $ produced by exposure to 35–50 mM $ K^{+} $. This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1β did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1β were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1β included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons. Conclusion Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1β at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1β may contribute to the central sensitization associated with chronic neuropathic pain. Dorsal Horn (dpeaa)DE-He213 Central Sensitization (dpeaa)DE-He213 Chronic Constriction Injury (dpeaa)DE-He213 Spare Nerve Injury (dpeaa)DE-He213 Delay Cell (dpeaa)DE-He213 Lu, Van B aut Lai, Aaron Y aut Todd, Kathryn G aut Ballanyi, Klaus aut Smith, Peter A aut Enthalten in Molecular pain London : Sage, 2005 4(2008), 1 vom: 17. Dez. (DE-627)47753368X (DE-600)2174252-2 1744-8069 nnns volume:4 year:2008 number:1 day:17 month:12 https://dx.doi.org/10.1186/1744-8069-4-63 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2008 1 17 12
spelling	10.1186/1744-8069-4-63 doi (DE-627)SPR029304334 (SPR)1744-8069-4-63-e DE-627 ger DE-627 rakwb eng Gustafson-Vickers, Sabrina L verfasserin aut Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gustafson-Vickers et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1β for 6–8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and $ Ca^{2+} $ imaging techniques. Results Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1β increased the change in intracellular $ Ca^{2+} $ produced by exposure to 35–50 mM $ K^{+} $. This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1β did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1β were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1β included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons. Conclusion Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1β at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1β may contribute to the central sensitization associated with chronic neuropathic pain. Dorsal Horn (dpeaa)DE-He213 Central Sensitization (dpeaa)DE-He213 Chronic Constriction Injury (dpeaa)DE-He213 Spare Nerve Injury (dpeaa)DE-He213 Delay Cell (dpeaa)DE-He213 Lu, Van B aut Lai, Aaron Y aut Todd, Kathryn G aut Ballanyi, Klaus aut Smith, Peter A aut Enthalten in Molecular pain London : Sage, 2005 4(2008), 1 vom: 17. Dez. (DE-627)47753368X (DE-600)2174252-2 1744-8069 nnns volume:4 year:2008 number:1 day:17 month:12 https://dx.doi.org/10.1186/1744-8069-4-63 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2008 1 17 12
allfields_unstemmed	10.1186/1744-8069-4-63 doi (DE-627)SPR029304334 (SPR)1744-8069-4-63-e DE-627 ger DE-627 rakwb eng Gustafson-Vickers, Sabrina L verfasserin aut Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gustafson-Vickers et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1β for 6–8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and $ Ca^{2+} $ imaging techniques. Results Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1β increased the change in intracellular $ Ca^{2+} $ produced by exposure to 35–50 mM $ K^{+} $. This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1β did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1β were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1β included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons. Conclusion Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1β at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1β may contribute to the central sensitization associated with chronic neuropathic pain. Dorsal Horn (dpeaa)DE-He213 Central Sensitization (dpeaa)DE-He213 Chronic Constriction Injury (dpeaa)DE-He213 Spare Nerve Injury (dpeaa)DE-He213 Delay Cell (dpeaa)DE-He213 Lu, Van B aut Lai, Aaron Y aut Todd, Kathryn G aut Ballanyi, Klaus aut Smith, Peter A aut Enthalten in Molecular pain London : Sage, 2005 4(2008), 1 vom: 17. Dez. (DE-627)47753368X (DE-600)2174252-2 1744-8069 nnns volume:4 year:2008 number:1 day:17 month:12 https://dx.doi.org/10.1186/1744-8069-4-63 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2008 1 17 12
allfieldsGer	10.1186/1744-8069-4-63 doi (DE-627)SPR029304334 (SPR)1744-8069-4-63-e DE-627 ger DE-627 rakwb eng Gustafson-Vickers, Sabrina L verfasserin aut Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gustafson-Vickers et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1β for 6–8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and $ Ca^{2+} $ imaging techniques. Results Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1β increased the change in intracellular $ Ca^{2+} $ produced by exposure to 35–50 mM $ K^{+} $. This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1β did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1β were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1β included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons. Conclusion Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1β at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1β may contribute to the central sensitization associated with chronic neuropathic pain. Dorsal Horn (dpeaa)DE-He213 Central Sensitization (dpeaa)DE-He213 Chronic Constriction Injury (dpeaa)DE-He213 Spare Nerve Injury (dpeaa)DE-He213 Delay Cell (dpeaa)DE-He213 Lu, Van B aut Lai, Aaron Y aut Todd, Kathryn G aut Ballanyi, Klaus aut Smith, Peter A aut Enthalten in Molecular pain London : Sage, 2005 4(2008), 1 vom: 17. Dez. (DE-627)47753368X (DE-600)2174252-2 1744-8069 nnns volume:4 year:2008 number:1 day:17 month:12 https://dx.doi.org/10.1186/1744-8069-4-63 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2008 1 17 12
allfieldsSound	10.1186/1744-8069-4-63 doi (DE-627)SPR029304334 (SPR)1744-8069-4-63-e DE-627 ger DE-627 rakwb eng Gustafson-Vickers, Sabrina L verfasserin aut Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gustafson-Vickers et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1β for 6–8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and $ Ca^{2+} $ imaging techniques. Results Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1β increased the change in intracellular $ Ca^{2+} $ produced by exposure to 35–50 mM $ K^{+} $. This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1β did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1β were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1β included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons. Conclusion Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1β at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1β may contribute to the central sensitization associated with chronic neuropathic pain. Dorsal Horn (dpeaa)DE-He213 Central Sensitization (dpeaa)DE-He213 Chronic Constriction Injury (dpeaa)DE-He213 Spare Nerve Injury (dpeaa)DE-He213 Delay Cell (dpeaa)DE-He213 Lu, Van B aut Lai, Aaron Y aut Todd, Kathryn G aut Ballanyi, Klaus aut Smith, Peter A aut Enthalten in Molecular pain London : Sage, 2005 4(2008), 1 vom: 17. Dez. (DE-627)47753368X (DE-600)2174252-2 1744-8069 nnns volume:4 year:2008 number:1 day:17 month:12 https://dx.doi.org/10.1186/1744-8069-4-63 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2704 GBV_ILN_2707 GBV_ILN_2890 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 4 2008 1 17 12
language	English
source	Enthalten in Molecular pain 4(2008), 1 vom: 17. Dez. volume:4 year:2008 number:1 day:17 month:12
sourceStr	Enthalten in Molecular pain 4(2008), 1 vom: 17. Dez. volume:4 year:2008 number:1 day:17 month:12
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topic_facet	Dorsal Horn Central Sensitization Chronic Constriction Injury Spare Nerve Injury Delay Cell
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container_title	Molecular pain
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author	Gustafson-Vickers, Sabrina L
spellingShingle	Gustafson-Vickers, Sabrina L misc Dorsal Horn misc Central Sensitization misc Chronic Constriction Injury misc Spare Nerve Injury misc Delay Cell Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization
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topic_title	Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization Dorsal Horn (dpeaa)DE-He213 Central Sensitization (dpeaa)DE-He213 Chronic Constriction Injury (dpeaa)DE-He213 Spare Nerve Injury (dpeaa)DE-He213 Delay Cell (dpeaa)DE-He213
topic	misc Dorsal Horn misc Central Sensitization misc Chronic Constriction Injury misc Spare Nerve Injury misc Delay Cell
topic_unstemmed	misc Dorsal Horn misc Central Sensitization misc Chronic Constriction Injury misc Spare Nerve Injury misc Delay Cell
topic_browse	misc Dorsal Horn misc Central Sensitization misc Chronic Constriction Injury misc Spare Nerve Injury misc Delay Cell
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title	Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization
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title_full	Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization
author_sort	Gustafson-Vickers, Sabrina L
journal	Molecular pain
journalStr	Molecular pain
lang_code	eng
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author_browse	Gustafson-Vickers, Sabrina L Lu, Van B Lai, Aaron Y Todd, Kathryn G Ballanyi, Klaus Smith, Peter A
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author-letter	Gustafson-Vickers, Sabrina L
doi_str_mv	10.1186/1744-8069-4-63
title_sort	long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization
title_auth	Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization
abstract	Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1β for 6–8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and $ Ca^{2+} $ imaging techniques. Results Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1β increased the change in intracellular $ Ca^{2+} $ produced by exposure to 35–50 mM $ K^{+} $. This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1β did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1β were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1β included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons. Conclusion Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1β at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1β may contribute to the central sensitization associated with chronic neuropathic pain. © Gustafson-Vickers et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1β for 6–8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and $ Ca^{2+} $ imaging techniques. Results Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1β increased the change in intracellular $ Ca^{2+} $ produced by exposure to 35–50 mM $ K^{+} $. This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1β did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1β were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1β included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons. Conclusion Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1β at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1β may contribute to the central sensitization associated with chronic neuropathic pain. © Gustafson-Vickers et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Background Cytokines such as interleukin 1β (IL-1β) have been implicated in the development of central sensitization that is characteristic of neuropathic pain. To examine its long-term effect on nociceptive processing, defined medium organotypic cultures of rat spinal cord were exposed to 100 pM IL-1β for 6–8 d. Interleukin effects in the dorsal horn were examined by whole-cell patch-clamp recording and $ Ca^{2+} $ imaging techniques. Results Examination of the cultures with confocal Fluo-4 AM imaging showed that IL-1β increased the change in intracellular $ Ca^{2+} $ produced by exposure to 35–50 mM $ K^{+} $. This is consistent with a modest increase in overall dorsal horn excitability. Despite this, IL-1β did not have a direct effect on rheobase or resting membrane potential nor did it selectively destroy any specific neuronal population. All effects were instead confined to changes in synaptic transmission. A variety of pre- and postsynaptic actions of IL-1β were seen in five different electrophysiologically-defined neuronal phenotypes. In putative excitatory 'delay' neurons, cytokine treatment increased the amplitude of spontaneous EPSC's (sEPSC) and decreased the frequency of spontaneous IPSC's (sIPSC). These effects would be expected to increase dorsal horn excitability and to facilitate the transfer of nociceptive information. However, other actions of IL-1β included disinhibition of putative inhibitory 'tonic' neurons and an increase in the amplitude of sIPSC's in 'delay' neurons. Conclusion Since spinal microglial activation peaks between 3 and 7 days after the initiation of chronic peripheral nerve injury and these cells release IL-1β at this time, our findings define some of the neurophysiological mechanisms whereby nerve-injury induced release of IL-1β may contribute to the central sensitization associated with chronic neuropathic pain. © Gustafson-Vickers et al; licensee BioMed Central Ltd. 2008. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Long-term actions of interleukin-1β on delay and tonic firing neurons in rat superficial dorsal horn and their relevance to central sensitization
url	https://dx.doi.org/10.1186/1744-8069-4-63
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