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Publication year
2012Source
European Journal of Pain, 16, 6, (2012), pp. 782-792ISSN
Publication type
Article / Letter to editor

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Organization
Anesthesiology
Neurophysiology
Former Organization
Cellular Animal Physiology
Journal title
European Journal of Pain
Volume
vol. 16
Issue
iss. 6
Page start
p. 782
Page end
p. 792
Subject
Neurophysiology; DCN MP - Plasticity and memory NCEBP 7: Effective primary care and public healthAbstract
Neuropathic pain is strongly associated with mood disorders like anxiety and depression. Corticotropin-releasing factor (CRF) plays a prominent role in these disorders as it is up-regulated in limbic structures such as the amygdala, upon experimentally induced neuropathy. This review discusses recent literature on the role of CRF in pain processing and highlights the amygdala as a potential hot spot in supraspinal descending pain control. Many studies have demonstrated analgesic effects of CRF following local and systemic administration, but more recently also hyperalgesic effects were shown upon endogenous amygdalar CRF increase or by blocking the CRF type 1 receptor (CRFR1). On the basis of the reviewed literature, we postulate a central mechanism for pain control in which the amygdala plays a critical role by switching on and off chronic pain. In this mechanism, upon pain stimuli, CRFR1 in the amygdala is activated by CRF to induce hyperalgesia. When the activated CRFR1 is internalized (pain initiation), it triggers the translocation of the cytoplasmic CRF type 2 receptor (CRFR2) to the plasma membrane. Here, CRFR2 can be recruited by either high (pharmacological) concentrations of CRF or by endogenous CRFR2 ligands, the urocortins, leading to analgesia (pain termination). This on-off switching of pain is completed by redistribution of the CRF receptors to their initial activity state. We furthermore propose that in neuropathic pain, this mechanism is dysregulated and causes a state of permanent hyperalgesia, and present an integrative (patho)physiological model for the way disturbed CRF receptor signalling in the amygdala could initiate neuropathic pain.
This item appears in the following Collection(s)
- Academic publications [205104]
- Electronic publications [103316]
- Faculty of Medical Sciences [81055]
- Faculty of Science [32347]
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