Limbic and HPA axis function in an animal model of chronic neuropathic pain

Ulrich‐Lai, Yvonne M.; Xie, Wenrui; Meij, Johanna T. A.; Dolgas, C. Mark; Yu, Lei; Herman, James P.

doi:10.1016/j.physbeh.2006.03.012

Cited by 124 publications

(101 citation statements)

References 69 publications

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“…CRF mRNA expression in the CeA increased in models of colitis pain (Greenwood-Van Meerveld et al, 2006) and neuropathic pain (Ulrich-Lai et al, 2006).…”

Section: Discussionmentioning

confidence: 97%

“…Previous biochemical (Sinniger et al, 2004;Greenwood-Van Meerveld et al, 2006;Ulrich-Lai et al, 2006) and behavioral (Lariviere and Melzack, 2000;McNally and Akil, 2002) studies point to the amygdala as an important site of CRF-mediated pain modulation, but the role of endogenously activated CRF1 and CRF2 receptors in the amygdala is not known. The present study used a multidisciplinary approach at the system and cellular levels to determine the effects of selective CRF1 and CRF2 receptor antagonists on pain-related synaptic facilitation in the amygdala, the underlying mechanisms and behavioral consequences.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Differential Mechanisms of CRF1 and CRF2 Receptor Functions in the Amygdala in Pain-Related Synaptic Facilitation and Behavior

Neugebauer²

2008

J. Neurosci.

160

231

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“…CRF mRNA expression in the CeA increased in models of colitis pain (Greenwood-Van Meerveld et al, 2006) and neuropathic pain (Ulrich-Lai et al, 2006).…”

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Differential Mechanisms of CRF1 and CRF2 Receptor Functions in the Amygdala in Pain-Related Synaptic Facilitation and Behavior

Neugebauer²

2008

J. Neurosci.

160

231

View full text Add to dashboard Cite

“…Previous electrophysiologycal [6], biochemical [43][44][45] and behavioral findings [18,27] have suggested that amygdaloid CRF receptors are involved in nociceptive modulation. The microinjection of a nonselective antagonist of CRF receptors in the amygdala reversed the hyperalgesia induced by opioid withdrawal as evaluated by the tail flick test in rats [27].…”

Section: Discussionmentioning

confidence: 99%

Activation of the corticotropin-releasing factor receptor from the basolateral or central amygdala modulates nociception in guinea pigs

Donatti¹,

Leite–Panissi²

2013

ABB

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Corticotropin-releasing factor (CRF) is a peptide that is released from the hypothalamus into widespread areas of the brain. Evidence has suggested that CRF is involved as a neuromodulator outside of the hypothalamic-pituitary-adrenal axis, playing an important role in fear, anxiety, depression and pain modulation. Our previous report demonstrated that CRF receptor activation in basolateral (BLA) or central nuclei of the amygdala (CeA) produces innate fear in guinea pigs. Inhibition of these receptors via administration of α-helical CRF 9-41 (a nonspecific antagonist) into the CeA or BLA decreased innate fear behavior [1]. Additionally, there is strong evidence that emotional behavior and nociception can be modulated simultaneously. The present study was conducted to investigate the involvement of the CRF receptors of the BLA or CeA in nociception in guinea pigs. Guinea pigs were treated with CRF and α-helical CRF9-41 in three different doses or injected with α-helical CRF 9-41 preceded by CRF into the BLA or CeA, and they were evaluated using the hot plate test. Our findings indicated that activation of CRF receptors in the BLA and in the CeA promoted antinociception, and this effect was reversed by preadministration of α-helical CRF 9-41 in the same area. The treatment with α-helical CRF 9-41 per se into the BLA and CeA did not alter nociception. Thus, nociception modulation occurs in a phasic manner, whereas defensive behavior can occur tonically because the α-helical CRF 9-41 did not cause any modification on the index of analgesia in the hot plate test but did reduce innate fear behavior [1].

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“…While it could be suggested that chronic pain may be a chronic inescapable stress (6), preclinical and clinical studies have shown that sustained neuropathic pain strongly differs from a simple stress regarding neuroendocrine hypothalamic-pituitaryadrenal (HPA) alterations, even if it induces similar behavioral consequences. Indeed, neuropathic pain does not modify the basal or stress-induced levels of corticosterone or the HPA axis negative feedback (4,7), while this is the case in the several models of stress-induced depression (8,9). Another hypothesis for pain-induced depression could be based on a shared neuroanatomical substrate, proposing that specific brain regions processing pain are also involved in moodrelated processing and that the alterations induced in these regions by chronic pain may alter the processing of affective information, thus resulting in mental disorders.…”

mentioning

confidence: 99%