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This study shows that peripheral mononeuropathy was accompanied by changes in limbic forebrain CRF<\/jats:styled-content>, but did not lead to changes in the functioning of the hypothalamo\u2010pituitary\u2013adrenal axis and the midbrain E<\/jats:styled-content>dinger\u2013W<\/jats:styled-content>estphal centrally projecting (EWcp<\/jats:styled-content>) neuron population, which play main roles in the organism's response to acute pain. Twenty\u2010four days after chronic constriction injury (CCI<\/jats:styled-content>) of the rat sciatic nerve, the oval bed nucleus of the stria terminalis (BSTov<\/jats:styled-content>) contained substantially more Crf<\/jats:italic> mRNA<\/jats:styled-content> as did the central amygdala (CeA<\/jats:styled-content>), which, in addition, possessed more CRF<\/jats:styled-content>. In contrast, Crf<\/jats:italic> mRNA<\/jats:styled-content> and CRF<\/jats:styled-content> contents of the hypothalamic paraventricular nucleus (PVN<\/jats:styled-content>) were unaffected by CCI<\/jats:styled-content>. Similarly, EWcp<\/jats:styled-content> neurons, producing the CRF<\/jats:styled-content> family member urocortin 1 (Ucn1<\/jats:styled-content>) and constitutively activated by various stressors including acute pain, did not show an effect of CCI<\/jats:styled-content> on Ucn1<\/jats:italic> mRNA<\/jats:styled-content> or Ucn1<\/jats:styled-content>. Also, the immediate early gene products cFos<\/jats:styled-content> and deltaFosB<\/jats:styled-content> in the EWcp<\/jats:styled-content> were unaffected by CCI<\/jats:styled-content>. These results indicate that neuropathic pain does not act via the HPA<\/jats:styled-content>\u2010axis or the EWcp<\/jats:styled-content>, but includes a main role of Crf<\/jats:styled-content><\/jats:italic> in the limbic system, which is in clear contrast to stressors like acute and chronic pain, which primarily act on the PVN<\/jats:styled-content> and the EWcp<\/jats:styled-content>.<\/jats:p>","DOI":"10.1016\/j.ejpain.2011.05.016","type":"journal-article","created":{"date-parts":[[2011,6,25]],"date-time":"2011-06-25T17:29:26Z","timestamp":1309022966000},"page":"61-71","source":"Crossref","is-referenced-by-count":43,"title":["Experimental neuropathy increases limbic forebrain CRF<\/scp>"],"prefix":"10.1002","volume":"16","author":[{"given":"T.","family":"Rouwette","sequence":"first","affiliation":[{"name":"Department of Cellular Animal Physiology Donders Institute for Brain, Cognition and Behaviour Centre for Neuroscience Radboud University Nijmegen Nijmegen The 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