Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia
<p>Abstract</p> <p>Activity-dependent synaptic plasticity is known to be important in learning and memory, persistent pain and drug addiction. Glutamate NMDA receptor activation stimulates several protein kinases, which then trigger biochemical cascades that lead to modifications i...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
SAGE Publishing
2006-06-01
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| Series: | Molecular Pain |
| Online Access: | http://www.molecularpain.com/content/2/1/21 |
| _version_ | 1818111393225768960 |
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| author | Tsien Joe Z Wang Huimin Shokat Kevan M Zhang Chao Wang Guo-Du Wei Feng Liauw Jason Zhuo Min |
| author_facet | Tsien Joe Z Wang Huimin Shokat Kevan M Zhang Chao Wang Guo-Du Wei Feng Liauw Jason Zhuo Min |
| author_sort | Tsien Joe Z |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Activity-dependent synaptic plasticity is known to be important in learning and memory, persistent pain and drug addiction. Glutamate NMDA receptor activation stimulates several protein kinases, which then trigger biochemical cascades that lead to modifications in synaptic efficacy. Genetic and pharmacological techniques have been used to show a role for Ca<sup>2+</sup>/calmodulin-dependent kinase II (CaMKII) in synaptic plasticity and memory formation. However, it is not known if increasing CaMKII activity in forebrain areas affects behavioral responses to tissue injury. Using genetic and pharmacological techniques, we were able to temporally and spatially restrict the over expression of CaMKII in forebrain areas. Here we show that genetic overexpression of CaMKII in the mouse forebrain selectively inhibits tissue injury-induced behavioral sensitization, including allodynia and hyperalgesia, while behavioral responses to acute noxious stimuli remain intact. CaMKII overexpression also inhibited synaptic depression induced by a prolonged repetitive stimulation in the ACC, suggesting an important role for CaMKII in the regulation of cingulate neurons. Our results suggest that neuronal CaMKII activity in the forebrain plays a role in persistent pain.</p> |
| first_indexed | 2024-12-11T03:02:20Z |
| format | Article |
| id | doaj.art-db94aefa0919432496820162b8363a26 |
| institution | Directory Open Access Journal |
| issn | 1744-8069 |
| language | English |
| last_indexed | 2024-12-11T03:02:20Z |
| publishDate | 2006-06-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Molecular Pain |
| spelling | doaj.art-db94aefa0919432496820162b8363a262022-12-22T01:23:01ZengSAGE PublishingMolecular Pain1744-80692006-06-01212110.1186/1744-8069-2-21Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesiaTsien Joe ZWang HuiminShokat Kevan MZhang ChaoWang Guo-DuWei FengLiauw JasonZhuo Min<p>Abstract</p> <p>Activity-dependent synaptic plasticity is known to be important in learning and memory, persistent pain and drug addiction. Glutamate NMDA receptor activation stimulates several protein kinases, which then trigger biochemical cascades that lead to modifications in synaptic efficacy. Genetic and pharmacological techniques have been used to show a role for Ca<sup>2+</sup>/calmodulin-dependent kinase II (CaMKII) in synaptic plasticity and memory formation. However, it is not known if increasing CaMKII activity in forebrain areas affects behavioral responses to tissue injury. Using genetic and pharmacological techniques, we were able to temporally and spatially restrict the over expression of CaMKII in forebrain areas. Here we show that genetic overexpression of CaMKII in the mouse forebrain selectively inhibits tissue injury-induced behavioral sensitization, including allodynia and hyperalgesia, while behavioral responses to acute noxious stimuli remain intact. CaMKII overexpression also inhibited synaptic depression induced by a prolonged repetitive stimulation in the ACC, suggesting an important role for CaMKII in the regulation of cingulate neurons. Our results suggest that neuronal CaMKII activity in the forebrain plays a role in persistent pain.</p>http://www.molecularpain.com/content/2/1/21 |
| spellingShingle | Tsien Joe Z Wang Huimin Shokat Kevan M Zhang Chao Wang Guo-Du Wei Feng Liauw Jason Zhuo Min Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia Molecular Pain |
| title | Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia |
| title_full | Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia |
| title_fullStr | Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia |
| title_full_unstemmed | Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia |
| title_short | Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia |
| title_sort | forebrain overexpression of camkii abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia |
| url | http://www.molecularpain.com/content/2/1/21 |
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