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α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia
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| Zeitschriftentitel: | Anesthesiology |
|---|---|
| Personen und Körperschaften: | , , , |
| In: | Anesthesiology, 101, 2004, 1, S. 185-190 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
|
| Schlagwörter: |
| author_facet |
Mansikka, Heikki Lähdesmäki, Janne Scheinin, Mika Pertovaara, Antti Mansikka, Heikki Lähdesmäki, Janne Scheinin, Mika Pertovaara, Antti |
|---|---|
| author |
Mansikka, Heikki Lähdesmäki, Janne Scheinin, Mika Pertovaara, Antti |
| spellingShingle |
Mansikka, Heikki Lähdesmäki, Janne Scheinin, Mika Pertovaara, Antti Anesthesiology α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia Anesthesiology and Pain Medicine |
| author_sort |
mansikka, heikki |
| spelling |
Mansikka, Heikki Lähdesmäki, Janne Scheinin, Mika Pertovaara, Antti 0003-3022 Ovid Technologies (Wolters Kluwer Health) Anesthesiology and Pain Medicine http://dx.doi.org/10.1097/00000542-200407000-00029 <jats:sec> <jats:title>Background</jats:title> <jats:p>Studies on receptor knockout mice have so far shown that of the three alpha2-adrenoceptor subtypes, the alpha(2A) adrenoceptor has a major role in mediating the powerful central analgesia induced by synthetic alpha2-adrenoceptor agonists. However, because a knockout of the gene for the alpha(2A) adrenoceptor has produced only little if any change in the pain sensitivity of control, nerve-injured, or inflamed animals, it has not been clear whether activation of alpha(2A)-adrenoceptors by endogenous ligands has a significant pain regulatory role.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>The authors assessed spontaneous pain behavior and mechanical hypersensitivity induced by administration of capsaicin in the colon or paw of alpha(2A)-adrenoceptor knockout mice versus their wild-type controls.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Enhanced pain hypersensitivity was observed in alpha(2A)-adrenoceptor knockout mice 20 min or more after administration of capsaicin, but before, hypersensitivity and spontaneous pain were of equal magnitude in alpha(2A)-adrenoceptor knockout and wild-type mice. When wild-type mice were pretreated with an alpha2-adrenoceptor antagonist, capsaicin-induced pain hypersensitivity increased to a level equal to that in alpha(2A)-adrenoceptor knockout mice. Capsaicin-induced hypersensitivity was suppressed in wild-type but not alpha(2A)-adrenoceptor knockout mice by a centrally acting alpha2-adrenoceptor agonist, whereas a peripherally acting alpha2-adrenoceptor agonist was without effect on hypersensitivity, although it attenuated capsaicin-induced spontaneous pain behavior in wild-type mice.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>This study shows that central alpha(2A)-adrenoceptors contribute to feedback inhibition of pain hypersensitivity. Also, alpha(2A)-adrenoceptors are critical for not only somatic but also visceral antinociceptive effects induced by synthetic alpha2-adrenoceptor agonists.</jats:p> </jats:sec> α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia Anesthesiology |
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Ovid Technologies (Wolters Kluwer Health), 2004 |
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Anesthesiology |
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| title |
α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_unstemmed |
α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_full |
α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_fullStr |
α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_full_unstemmed |
α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_short |
α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_sort |
α2aadrenoceptors contribute to feedback inhibition of capsaicin-induced hyperalgesia |
| topic |
Anesthesiology and Pain Medicine |
| url |
http://dx.doi.org/10.1097/00000542-200407000-00029 |
| publishDate |
2004 |
| physical |
185-190 |
| description |
<jats:sec>
<jats:title>Background</jats:title>
<jats:p>Studies on receptor knockout mice have so far shown that of the three alpha2-adrenoceptor subtypes, the alpha(2A) adrenoceptor has a major role in mediating the powerful central analgesia induced by synthetic alpha2-adrenoceptor agonists. However, because a knockout of the gene for the alpha(2A) adrenoceptor has produced only little if any change in the pain sensitivity of control, nerve-injured, or inflamed animals, it has not been clear whether activation of alpha(2A)-adrenoceptors by endogenous ligands has a significant pain regulatory role.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Methods</jats:title>
<jats:p>The authors assessed spontaneous pain behavior and mechanical hypersensitivity induced by administration of capsaicin in the colon or paw of alpha(2A)-adrenoceptor knockout mice versus their wild-type controls.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Results</jats:title>
<jats:p>Enhanced pain hypersensitivity was observed in alpha(2A)-adrenoceptor knockout mice 20 min or more after administration of capsaicin, but before, hypersensitivity and spontaneous pain were of equal magnitude in alpha(2A)-adrenoceptor knockout and wild-type mice. When wild-type mice were pretreated with an alpha2-adrenoceptor antagonist, capsaicin-induced pain hypersensitivity increased to a level equal to that in alpha(2A)-adrenoceptor knockout mice. Capsaicin-induced hypersensitivity was suppressed in wild-type but not alpha(2A)-adrenoceptor knockout mice by a centrally acting alpha2-adrenoceptor agonist, whereas a peripherally acting alpha2-adrenoceptor agonist was without effect on hypersensitivity, although it attenuated capsaicin-induced spontaneous pain behavior in wild-type mice.</jats:p>
</jats:sec>
<jats:sec>
<jats:title>Conclusions</jats:title>
<jats:p>This study shows that central alpha(2A)-adrenoceptors contribute to feedback inhibition of pain hypersensitivity. Also, alpha(2A)-adrenoceptors are critical for not only somatic but also visceral antinociceptive effects induced by synthetic alpha2-adrenoceptor agonists.</jats:p>
</jats:sec> |
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| author | Mansikka, Heikki, Lähdesmäki, Janne, Scheinin, Mika, Pertovaara, Antti |
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| description | <jats:sec> <jats:title>Background</jats:title> <jats:p>Studies on receptor knockout mice have so far shown that of the three alpha2-adrenoceptor subtypes, the alpha(2A) adrenoceptor has a major role in mediating the powerful central analgesia induced by synthetic alpha2-adrenoceptor agonists. However, because a knockout of the gene for the alpha(2A) adrenoceptor has produced only little if any change in the pain sensitivity of control, nerve-injured, or inflamed animals, it has not been clear whether activation of alpha(2A)-adrenoceptors by endogenous ligands has a significant pain regulatory role.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>The authors assessed spontaneous pain behavior and mechanical hypersensitivity induced by administration of capsaicin in the colon or paw of alpha(2A)-adrenoceptor knockout mice versus their wild-type controls.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Enhanced pain hypersensitivity was observed in alpha(2A)-adrenoceptor knockout mice 20 min or more after administration of capsaicin, but before, hypersensitivity and spontaneous pain were of equal magnitude in alpha(2A)-adrenoceptor knockout and wild-type mice. When wild-type mice were pretreated with an alpha2-adrenoceptor antagonist, capsaicin-induced pain hypersensitivity increased to a level equal to that in alpha(2A)-adrenoceptor knockout mice. Capsaicin-induced hypersensitivity was suppressed in wild-type but not alpha(2A)-adrenoceptor knockout mice by a centrally acting alpha2-adrenoceptor agonist, whereas a peripherally acting alpha2-adrenoceptor agonist was without effect on hypersensitivity, although it attenuated capsaicin-induced spontaneous pain behavior in wild-type mice.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>This study shows that central alpha(2A)-adrenoceptors contribute to feedback inhibition of pain hypersensitivity. Also, alpha(2A)-adrenoceptors are critical for not only somatic but also visceral antinociceptive effects induced by synthetic alpha2-adrenoceptor agonists.</jats:p> </jats:sec> |
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| physical | 185-190 |
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| spelling | Mansikka, Heikki Lähdesmäki, Janne Scheinin, Mika Pertovaara, Antti 0003-3022 Ovid Technologies (Wolters Kluwer Health) Anesthesiology and Pain Medicine http://dx.doi.org/10.1097/00000542-200407000-00029 <jats:sec> <jats:title>Background</jats:title> <jats:p>Studies on receptor knockout mice have so far shown that of the three alpha2-adrenoceptor subtypes, the alpha(2A) adrenoceptor has a major role in mediating the powerful central analgesia induced by synthetic alpha2-adrenoceptor agonists. However, because a knockout of the gene for the alpha(2A) adrenoceptor has produced only little if any change in the pain sensitivity of control, nerve-injured, or inflamed animals, it has not been clear whether activation of alpha(2A)-adrenoceptors by endogenous ligands has a significant pain regulatory role.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>The authors assessed spontaneous pain behavior and mechanical hypersensitivity induced by administration of capsaicin in the colon or paw of alpha(2A)-adrenoceptor knockout mice versus their wild-type controls.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Enhanced pain hypersensitivity was observed in alpha(2A)-adrenoceptor knockout mice 20 min or more after administration of capsaicin, but before, hypersensitivity and spontaneous pain were of equal magnitude in alpha(2A)-adrenoceptor knockout and wild-type mice. When wild-type mice were pretreated with an alpha2-adrenoceptor antagonist, capsaicin-induced pain hypersensitivity increased to a level equal to that in alpha(2A)-adrenoceptor knockout mice. Capsaicin-induced hypersensitivity was suppressed in wild-type but not alpha(2A)-adrenoceptor knockout mice by a centrally acting alpha2-adrenoceptor agonist, whereas a peripherally acting alpha2-adrenoceptor agonist was without effect on hypersensitivity, although it attenuated capsaicin-induced spontaneous pain behavior in wild-type mice.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>This study shows that central alpha(2A)-adrenoceptors contribute to feedback inhibition of pain hypersensitivity. Also, alpha(2A)-adrenoceptors are critical for not only somatic but also visceral antinociceptive effects induced by synthetic alpha2-adrenoceptor agonists.</jats:p> </jats:sec> α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia Anesthesiology |
| spellingShingle | Mansikka, Heikki, Lähdesmäki, Janne, Scheinin, Mika, Pertovaara, Antti, Anesthesiology, α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia, Anesthesiology and Pain Medicine |
| title | α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_full | α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_fullStr | α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_full_unstemmed | α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_short | α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| title_sort | α2aadrenoceptors contribute to feedback inhibition of capsaicin-induced hyperalgesia |
| title_unstemmed | α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia |
| topic | Anesthesiology and Pain Medicine |
| url | http://dx.doi.org/10.1097/00000542-200407000-00029 |