{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T18:47:45Z","timestamp":1791053265198,"version":"4.1.0"},"reference-count":75,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2011,12,19]],"date-time":"2011-12-19T00:00:00Z","timestamp":1324252800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European Journal of Pain"],"published-print":{"date-parts":[[2012,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Pain markedly activates the hypothalamic\u2010pituitary\u2010adrenal (\n                      <jats:styled-content style=\"fixed-case\">HPA<\/jats:styled-content>\n                      ) axis and increases plasma corticosterone release interfering significantly with nociceptive behaviour as well as the mechanism of action of analgesic drugs.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aims\/Methods<\/jats:title>\n                    <jats:p>\n                      In the present study, we monitored the time course of circulating corticosterone in two mouse strains (\n                      <jats:styled-content style=\"fixed-case\">C57Bl\/6<\/jats:styled-content>\n                      and\n                      <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\n                      alb\/\n                      <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>\n                      ) under different pain models. In addition, the stress response was investigated following animal handling, intrathecal (i.t.) manipulation and habituation to environmental conditions commonly used in nociceptive experimental assays. We also examined the influence of within\u2010cage order of testing on plasma corticosterone.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Subcutaneous injection of capsaicin precipitated a prompt stress response whereas carrageenan and complete Freund's adjuvant induced an increased corticosterone release around the third hour post\u2010injection. However, carrageenan induced a longer increased corticosterone in\n                      <jats:styled-content style=\"fixed-case\">C57Bl\/6<\/jats:styled-content>\n                      mice. In partial sciatic nerve ligation, neuropathic pain model corticosterone increased only in the first days whereas mechanical hypersensitivity remained much longer. Animal handling also represents an important stressor whereas the i.t. injection per se does not exacerbate the handling\u2010induced stress response. Moreover, the order of testing animals from the same cage does not interfere with plasma corticosterone levels in the intrathecal procedure. Animal habituation to the testing apparatus also does not reduce the immediate corticosterone increase as compared with non\u2010habituated mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Our data indicate that\n                      <jats:styled-content style=\"fixed-case\">HPA<\/jats:styled-content>\n                      axis activation in acute and chronic pain models is time dependent and may be dissociated from evoked hyperalgesia. Therefore,\n                      <jats:styled-content style=\"fixed-case\">HPA<\/jats:styled-content>\n                      \u2010axis activation represents an important variable to be considered when designing experimental assays of persistent pain as well as for interpretation of data.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/j.1532-2149.2011.00066.x","type":"journal-article","created":{"date-parts":[[2011,12,22]],"date-time":"2011-12-22T06:39:39Z","timestamp":1324535979000},"page":"803-815","source":"Crossref","is-referenced-by-count":60,"title":["Plasma corticosterone levels in mouse models of pain"],"prefix":"10.1002","volume":"16","author":[{"given":"M.","family":"Benedetti","sequence":"first","affiliation":[{"name":"Department of Neuroscience and Behaviour Ribeir\u00e3o Preto School of Medicine University of S\u00e3o Paulo  Av. Bandeirantes, 3900 Ribeir\u00e3o Preto SP 14049\u2010900 Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Merino","sequence":"additional","affiliation":[{"name":"Department of Neuroscience and Behaviour Ribeir\u00e3o Preto School of Medicine University of S\u00e3o Paulo  Av. Bandeirantes, 3900 Ribeir\u00e3o Preto SP 14049\u2010900 Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Kusuda","sequence":"additional","affiliation":[{"name":"Department of Physiology Ribeir\u00e3o Preto School of Medicine University of S\u00e3o Paulo  Av. Bandeirantes, 3900 Ribeir\u00e3o Preto SP 14049\u2010900 Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.I.","family":"Ravanelli","sequence":"additional","affiliation":[{"name":"Department of Physiology Ribeir\u00e3o Preto School of Medicine University of S\u00e3o Paulo  Av. 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