Involvement of spinal kappa opioid receptors in the antiociception produced by intrathecaliy administered corticotropin-releasing factor in mice

Song, Zhijing; Takemori, A. E.

doi:10.1016/0014-2999(90)94590-t

Cited by 9 publications

(19 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results corroborate the present study, where the administration of CRF in the BLA and CeA promoted an antinociceptive effect that was reversed by the pre-administration of a CRF receptor antagonist (α-helical CRF [9][10][11][12][13][14][15][16][17][18][19][20][21] ) in the same areas. Our previous report also demonstrated that the activation of CRF receptors in the BLA or CeA potentiates a tonic immobility response (a defensive behavior associated with innate fear and/or anxiety) in guinea pigs [1].…”

Section: Discussionsupporting

confidence: 79%

See 1 more Smart Citation

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

Donatti¹,

Leite–Panissi²

2013

ABB

View full text Add to dashboard Cite

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].

show abstract

Section: Discussionsupporting

confidence: 79%

“…Furthermore, antinociception has been shown (7) 礸 0.5 CRF (7) 礸 1.0 CRF (7) a-h-CRF 9-41 + CRF ( to be induced by different routes of administration, including intracerebroventricular, intrathecal, and intracisternal [19][20][21]. However, the mechanisms by which this peptide acts are still unclear [22].…”

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

View full text Add to dashboard Cite

show abstract

“…Peripheral CRF treatment in humans mimics central CRF treatment in rats: induction of abdominal pain or discomfort 22 and facilitated perception to rectal distension 23 . In contrast, other reports show that central or systemic injection of CRF in rodents induces antinociceptive actions on visceral pain, which can be antagonized by a CRF 1,2 antagonist 24,25 . We hypothesized that these divergent effects of CRF are explained by selective activation of the CRF 1 and CRF 2 receptor.…”

Section: Introductionmentioning

confidence: 90%

Divergent role for CRF₁ and CRF₂ receptors in the modulation of visceral pain

Nijsen

Ongenae

Meulemans

et al. 2005

Neurogastroenterology Motil

View full text Add to dashboard Cite

Both anti- and pro-nociceptive effects of corticotropin-releasing factor (CRF) treatment on visceral pain have been reported. Here, this dual action of CRF was differentiated by selective (in)activation of the CRF1 and CRF2 receptor prior to a visceral pain stimulus. Visceral pain was evaluated out of behavioural and visceromotor (abdominal electromyogram) responses to duodenal distension in the freely moving rat. Intraperitoneal (i.p.) CRF (50 microg kg-1) increased the distension-induced visceromotor and behavioural pain response. The pro-nociceptive effects of CRF on the behavioural response were attenuated by a selective CRF1 (CP-154526; 20 mg kg-1) but not a selective CRF2 [antiSauvagine30 (aSVG30); 100 microg kg-1] antagonist. Selective activation of the CRF2 receptor by stresscopin-related peptide (SRP; i.p. 25 microg kg-1) reduced the distension-induced visceromotor and behavioural response. Intrathecal injection of CRF (2 microg 10 microL-1) or SRP (20 microg 10 microL-1) decreased the distension-induced visceromotor and behavioural response. The antinociceptive effects of intrathecal CRF on the behavioural response were attenuated by aSVG30 (20 microg 10 microL-1) but not with CP-154526 (10 microg 10 microL-1). These findings indicate that the CRF1 receptor is involved in pro-nociception of visceral pain, whereas the CRF2 receptor is mainly involved in antinociception. This divergent role of the CRF subreceptors may explain the bimodal effects of CRF treatment on visceral nociception.

show abstract

“…Only two studies suggested antinociceptive effects following intrathecal (i.t.) CRF administration in visceral pain (Song and Takemori, 1991;Nijsen et al, 2005). Several other studies showed no robust results about CRF's modulation of nociception following its central or sytemic application (Lariviere and Melzack, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…We further examined whether CRF-mediated alterations in inflammatory pain were specifically reversed by a CRF receptor antagonist at the anatomical site of CRF's application. As some previous studies suggested a possible involvement of endogenous opioid peptides (Hargreaves et al, 1987;Song and Takemori, 1990), we also investigated whether CRF's antinociception is attenuated by the local application of the opioid receptor antagonist naloxone. In parallel to our behavioral experiments, we aimed at identifying potential, pain-relevant anatomical sites of CRF's action, which coexpress both CRF receptors and opioid peptides within the brain, the dorsal horn of the spinal cord and within peripheral tissue using immunohistochemistry.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Mousa

Bopaiah

Richter

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

There is conflicting evidence on the antinociceptive effects of corticotropin-releasing factor (CRF) along the neuraxis of pain transmission and the responsible anatomical sites of CRF's action at the level of the brain, spinal cord and periphery. In an animal model of tonic pain, that is, Freunds complete adjuvant (FCA) hindpaw inflammation, we systematically investigated CRF's ability to modulate inflammatory pain at those three levels of pain transmission by algesiometry following the intracerebroventricular, intrathecal, and intraplantar application of low, systemically inactive doses of CRF. At each level, CRF elicits potent antinociceptive effects, which are dose dependent and antagonized by local, but not systemic CRF receptor antagonist a-helical CRF indicating CRF receptor specificity. Consistently, we have identified by immunohistochemistry multiple brain areas, inhibitory interneurons within the dorsal horn of the spinal cord as well as immune cells within subcutaneous tissueFbut not peripheral sensory neuronsFthat coexpress both CRF receptors and opioid peptides. In line with these anatomical findings, local administration of CRF together with the opioid receptor antagonist naloxone dosedependently reversed CRF's antinociceptive effects at each of these three levels of pain transmission. Therefore, local application of low, systemically inactive doses of CRF at the level of the brain, spinal cord and periphery inhibits tonic inflammatory pain most likely through an activation of CRF receptors on cells that coexpress opioid peptides which results in opioid-mediated pain inhibition. Future studies have to delineate whether endogenous CRF at these three levels contributes to the body's response to cope with the stressful stimulus pain in an opioid-mediated manner.

show abstract

Involvement of spinal kappa opioid receptors in the antiociception produced by intrathecaliy administered corticotropin-releasing factor in mice

Cited by 9 publications

References 0 publications

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

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

Divergent role for CRF₁ and CRF₂ receptors in the modulation of visceral pain

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Contact Info

Product

Resources

About

Involvement of spinal kappa opioid receptors in the antiociception produced by intrathecaliy administered corticotropin-releasing factor in mice

Cited by 9 publications

References 0 publications

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

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

Divergent role for CRF1 and CRF2 receptors in the modulation of visceral pain

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Contact Info

Product

Resources

About

Divergent role for CRF₁ and CRF₂ receptors in the modulation of visceral pain