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Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis
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| Zeitschriftentitel: | CNS Neuroscience & Therapeutics |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | CNS Neuroscience & Therapeutics, 19, 2013, 1, S. 12-19 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Yan, Hai‐Tao Wu, Ning Lu, Xin‐Qiang Su, Rui‐Bin Zheng, Jian‐Quan Li, Jin Yan, Hai‐Tao Wu, Ning Lu, Xin‐Qiang Su, Rui‐Bin Zheng, Jian‐Quan Li, Jin |
|---|---|
| author |
Yan, Hai‐Tao Wu, Ning Lu, Xin‐Qiang Su, Rui‐Bin Zheng, Jian‐Quan Li, Jin |
| spellingShingle |
Yan, Hai‐Tao Wu, Ning Lu, Xin‐Qiang Su, Rui‐Bin Zheng, Jian‐Quan Li, Jin CNS Neuroscience & Therapeutics Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology |
| author_sort |
yan, hai‐tao |
| spelling |
Yan, Hai‐Tao Wu, Ning Lu, Xin‐Qiang Su, Rui‐Bin Zheng, Jian‐Quan Li, Jin 1755-5930 1755-5949 Wiley Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology http://dx.doi.org/10.1111/cns.12012 <jats:title>Summary</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Glutamate homeostasis plays a critical role in mediating the addiction‐related behaviors. Therefore, preventing the disruption or reestablishing of it is a novel strategy for the treatment of addiction. Glutamate transporters are responsible for clearing extracellular glutamate and maintaining glutamate homeostasis. Our previous work demonstrated that aquaporin‐4 (<jats:styled-content style="fixed-case">AQP</jats:styled-content>4) deficiency attenuated morphine dependence, but the mechanisms are unclear. According to the recent evidence that <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 might form a functional complex with glutamate transporter‐1 (<jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1), this study focused on whether <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 participates in the modulation of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 and glutamate homeostasis in morphine‐dependent mice.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>We found that <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout prevented the down‐regulations of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 expression and glutamate clearance when mice were repeatedly treated with morphine. Further study revealed that inhibition of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 by dihydrokainic acid (<jats:styled-content style="fixed-case">DHK</jats:styled-content>) initiated morphine dependence in <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout mice. In addition, <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout abolished both decreases and increases in the extracellular glutamate levels in the prefrontal cortex during repeated morphine treatment and naloxone‐precipitated withdrawal.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p><jats:styled-content style="fixed-case">AQP</jats:styled-content>4 deficiency suppresses the down‐regulation of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1, and the disruption of glutamate homeostasis caused by repeated exposure to morphine, pointing to a strategy for maintaining glutamate homeostasis and thereby treating addiction through the modulation of <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 function and expression.</jats:p></jats:sec> Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis CNS Neuroscience & Therapeutics |
| doi_str_mv |
10.1111/cns.12012 |
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Online Free |
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Chemie und Pharmazie Biologie Medizin Psychologie |
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Wiley, 2013 |
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Wiley, 2013 |
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yan2013aquaporin4deficiencyattenuatesopioiddependencethroughsuppressingglutamatetransporter1downregulationandmaintainingglutamatehomeostasis |
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2013 |
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Wiley |
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CNS Neuroscience & Therapeutics |
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49 |
| title |
Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_unstemmed |
Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_full |
Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_fullStr |
Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_full_unstemmed |
Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_short |
Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_sort |
aquaporin‐4 deficiency attenuates opioid dependence through suppressing glutamate transporter‐1 down‐regulation and maintaining glutamate homeostasis |
| topic |
Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology |
| url |
http://dx.doi.org/10.1111/cns.12012 |
| publishDate |
2013 |
| physical |
12-19 |
| description |
<jats:title>Summary</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Glutamate homeostasis plays a critical role in mediating the addiction‐related behaviors. Therefore, preventing the disruption or reestablishing of it is a novel strategy for the treatment of addiction. Glutamate transporters are responsible for clearing extracellular glutamate and maintaining glutamate homeostasis. Our previous work demonstrated that aquaporin‐4 (<jats:styled-content style="fixed-case">AQP</jats:styled-content>4) deficiency attenuated morphine dependence, but the mechanisms are unclear. According to the recent evidence that <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 might form a functional complex with glutamate transporter‐1 (<jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1), this study focused on whether <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 participates in the modulation of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 and glutamate homeostasis in morphine‐dependent mice.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>We found that <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout prevented the down‐regulations of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 expression and glutamate clearance when mice were repeatedly treated with morphine. Further study revealed that inhibition of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 by dihydrokainic acid (<jats:styled-content style="fixed-case">DHK</jats:styled-content>) initiated morphine dependence in <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout mice. In addition, <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout abolished both decreases and increases in the extracellular glutamate levels in the prefrontal cortex during repeated morphine treatment and naloxone‐precipitated withdrawal.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p><jats:styled-content style="fixed-case">AQP</jats:styled-content>4 deficiency suppresses the down‐regulation of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1, and the disruption of glutamate homeostasis caused by repeated exposure to morphine, pointing to a strategy for maintaining glutamate homeostasis and thereby treating addiction through the modulation of <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 function and expression.</jats:p></jats:sec> |
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| author | Yan, Hai‐Tao, Wu, Ning, Lu, Xin‐Qiang, Su, Rui‐Bin, Zheng, Jian‐Quan, Li, Jin |
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| description | <jats:title>Summary</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Glutamate homeostasis plays a critical role in mediating the addiction‐related behaviors. Therefore, preventing the disruption or reestablishing of it is a novel strategy for the treatment of addiction. Glutamate transporters are responsible for clearing extracellular glutamate and maintaining glutamate homeostasis. Our previous work demonstrated that aquaporin‐4 (<jats:styled-content style="fixed-case">AQP</jats:styled-content>4) deficiency attenuated morphine dependence, but the mechanisms are unclear. According to the recent evidence that <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 might form a functional complex with glutamate transporter‐1 (<jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1), this study focused on whether <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 participates in the modulation of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 and glutamate homeostasis in morphine‐dependent mice.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>We found that <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout prevented the down‐regulations of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 expression and glutamate clearance when mice were repeatedly treated with morphine. Further study revealed that inhibition of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 by dihydrokainic acid (<jats:styled-content style="fixed-case">DHK</jats:styled-content>) initiated morphine dependence in <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout mice. In addition, <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout abolished both decreases and increases in the extracellular glutamate levels in the prefrontal cortex during repeated morphine treatment and naloxone‐precipitated withdrawal.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p><jats:styled-content style="fixed-case">AQP</jats:styled-content>4 deficiency suppresses the down‐regulation of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1, and the disruption of glutamate homeostasis caused by repeated exposure to morphine, pointing to a strategy for maintaining glutamate homeostasis and thereby treating addiction through the modulation of <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 function and expression.</jats:p></jats:sec> |
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| spelling | Yan, Hai‐Tao Wu, Ning Lu, Xin‐Qiang Su, Rui‐Bin Zheng, Jian‐Quan Li, Jin 1755-5930 1755-5949 Wiley Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology http://dx.doi.org/10.1111/cns.12012 <jats:title>Summary</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Glutamate homeostasis plays a critical role in mediating the addiction‐related behaviors. Therefore, preventing the disruption or reestablishing of it is a novel strategy for the treatment of addiction. Glutamate transporters are responsible for clearing extracellular glutamate and maintaining glutamate homeostasis. Our previous work demonstrated that aquaporin‐4 (<jats:styled-content style="fixed-case">AQP</jats:styled-content>4) deficiency attenuated morphine dependence, but the mechanisms are unclear. According to the recent evidence that <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 might form a functional complex with glutamate transporter‐1 (<jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1), this study focused on whether <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 participates in the modulation of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 and glutamate homeostasis in morphine‐dependent mice.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>We found that <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout prevented the down‐regulations of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 expression and glutamate clearance when mice were repeatedly treated with morphine. Further study revealed that inhibition of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1 by dihydrokainic acid (<jats:styled-content style="fixed-case">DHK</jats:styled-content>) initiated morphine dependence in <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout mice. In addition, <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 knockout abolished both decreases and increases in the extracellular glutamate levels in the prefrontal cortex during repeated morphine treatment and naloxone‐precipitated withdrawal.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p><jats:styled-content style="fixed-case">AQP</jats:styled-content>4 deficiency suppresses the down‐regulation of <jats:styled-content style="fixed-case">GLT</jats:styled-content>‐1, and the disruption of glutamate homeostasis caused by repeated exposure to morphine, pointing to a strategy for maintaining glutamate homeostasis and thereby treating addiction through the modulation of <jats:styled-content style="fixed-case">AQP</jats:styled-content>4 function and expression.</jats:p></jats:sec> Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis CNS Neuroscience & Therapeutics |
| spellingShingle | Yan, Hai‐Tao, Wu, Ning, Lu, Xin‐Qiang, Su, Rui‐Bin, Zheng, Jian‐Quan, Li, Jin, CNS Neuroscience & Therapeutics, Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis, Pharmacology (medical), Physiology (medical), Psychiatry and Mental health, Pharmacology |
| title | Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_full | Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_fullStr | Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_full_unstemmed | Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_short | Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| title_sort | aquaporin‐4 deficiency attenuates opioid dependence through suppressing glutamate transporter‐1 down‐regulation and maintaining glutamate homeostasis |
| title_unstemmed | Aquaporin‐4 Deficiency Attenuates Opioid Dependence through Suppressing Glutamate Transporter‐1 Down‐regulation and Maintaining Glutamate Homeostasis |
| topic | Pharmacology (medical), Physiology (medical), Psychiatry and Mental health, Pharmacology |
| url | http://dx.doi.org/10.1111/cns.12012 |