Central CRH administration changes formalin pain responses in male and female rats

Lariviere, William R.; Fiorenzani, Paolo; Ceccarelli, Ilaria; Massafra, C; Sorda, Giuseppina; Canio, Clara Di; Aloisi, Anna Maria

doi:10.1016/j.brainres.2011.01.106

Cited by 18 publications

(11 citation statements)

References 35 publications

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“…More recent studies have attempted to reconcile these differences, with significant progress. For example, Lariviere et al (2011) revealed differential effects of central CRF on distinct behavioral responses in the formalin test. Additionally, with the development of more selective pharmacological tools for distinguishing specific CRF receptor-subtype function, recent work suggests that the central anti-nociceptive effects of CRF are most likely mediated through CRF 2 receptors (Ji and Neugebauer, 2008).…”

Section: Discussionmentioning

confidence: 99%

Development of mechanical hypersensitivity in rats during heroin and ethanol dependence: Alleviation by CRF1 receptor antagonism

et al. 2012

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Animal models of drug dependence have described both reductions in brain reward processes and potentiation of stress-like (or anti-reward) mechanisms, including a recruitment of corticotropin-releasing factor (CRF) signaling. Accordingly, chronic exposure to opiates often leads to the development of mechanical hypersensitivity. We measured paw withdrawal thresholds (PWTs) in male Wistar rats allowed limited (short access group: ShA) or extended (long access group: LgA) access to heroin or cocaine self-administration, or in rats made dependent on ethanol via ethanol vapor exposure (ethanol-dependent group). In heroin self-administering animals, after transition to LgA conditions, thresholds were reduced to around 50% of levels observed at baseline, and were also significantly lower than thresholds measured in animals remaining on the ShA schedule. In contrast, thresholds in animals self-administering cocaine under either ShA (1 h) or LgA (6 h) conditions were unaltered. Similar to heroin LgA rats, ethanol-dependent rats also developed mechanical hypersensitivity after eight weeks of ethanol vapor exposure compared to non-dependent animals. Systemic administration of the CRF1R antagonist MPZP significantly alleviated the hypersensitivity observed in rats dependent on heroin or ethanol. The emergence of mechanical hypersensitivity with heroin and ethanol dependence may thus represent one critical drug-associated negative emotional state driving dependence on these substances. These results also suggest a recruitment of CRF-regulated nociceptive pathways associated with escalation of intake and dependence. A greater understanding of relationships between chronic drug exposure and pain-related states may provide insight into mechanisms underlying the transition to drug addiction, as well as reveal new treatment opportunities.

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Section: Discussionmentioning

confidence: 99%

Development of mechanical hypersensitivity in rats during heroin and ethanol dependence: Alleviation by CRF1 receptor antagonism

et al. 2012

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“…CRF administration was shown to cause analgesia during the interphase of pain stimulation by formalin application, but did not show an effect during the first or second phase of this test (Vit et al., ). Antinociceptive effects of CRF administration during the interphase of the formalin test were also demonstrated in male and female rats (Lariviere et al., ), which indicates that CRF is antinociceptive by activating descending pain inhibitory circuits to the spinal cord. However, rats showed an increase in licking behaviour during the first and second phases of the test, indicating a hyperalgesic effect of CRF during these phases (Lariviere et al., ).…”

Section: Crfmentioning

confidence: 91%

“…However, in the past decade, the role of CRF in the CNS in pain and analgesia gained increasing attention. It has become clear that the peptide has pleiotropic effects: it can induce analgesia but in some rodent pain models opposite, hyperalgesic effects of CRF have been shown (Bourbia et al., ; Lariviere et al., ). To substantiate the significance of forebrain CRF in pain behaviour, we will first discuss the CNS effects of CRF and CRF (receptor) antagonists on pain behaviour.…”

Section: Crfmentioning

confidence: 99%

The amygdala, a relay station for switching on and off pain

Rouwette

Vanelderen

Roubos

et al. 2011

European Journal of Pain

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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.

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“…On the other hand, evidences showed that NO and ONOO − facilitate PGE 2 -induced hyperalgesia, but has lower hyperalgesic action when acting alone (Ndengele et al, 2008). The injection of dilute formalin produces a persistent biphasic nociceptive stimulation noted by the behavioral pain responses of licking, flexing and jerking of the injected paw (Lariviere et al, 2011). The early phase of response (within 0-5 min after injection) comprises the neurogenic pain, while the late phase (within 15-60 min after injection) comprises the inflammatory pain (hyperalgesia) (Lapa et al, 2008).…”

Section: Resultsmentioning

confidence: 97%

Anti-inflammatory action of Justicia acuminatissima leaves

Verdam

Guilhon-Simplicio

Barbosa

et al. 2015

Revista Brasileira de Farmacognosia

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BJP 122 1-5 Revista Brasileira de Farmacognosia xxx (2015) xxx-xxx w w w . s b f g n o s i a . o r g . b r / r e v i s t a a b s t r a c t In Amazonas State (Brazil), Justicia acuminatissima (Miq.) Bremek., Acanthaceae, leaf teas are used in folk medicine to treat several inflammatory illnesses. In order to validate this medicinal application, we analyzed the acute toxicity and antioxidant, antiedematogenic and antinociceptive potentials of an aqueous extract of this species, using culture cells and animal models. The aqueous extract did not cause toxic effects on human lymphocytes in high concentration (400 g/mL), neither on mice treated with high doses (5000 mg/kg) in an acute toxicity analysis by oral route, and also did not cause lesions in the gastric mucosa of animals treated with 300 mg/kg, which was the maximal dose used in the anti-inflammatory screening. The aqueous extract caused inhibition of inflammatory pain in formalin-induced paw licking test with all tested doses, 30, 100 and 300 mg/kg, and antiedematogenic activity at 100 and 300 mg/kg. Additionally, the aqueous extract presented statistically significant action on the release of nitric oxide by lipopolysaccharide-activated macrophages. These results and other previously observed preliminarily Q2 studies support the folk use of this species, and further investigation of its action mechanism by inhibition of COX-2 or related metabolite would be interesting.

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Central CRH administration changes formalin pain responses in male and female rats

Cited by 18 publications

References 35 publications

Development of mechanical hypersensitivity in rats during heroin and ethanol dependence: Alleviation by CRF1 receptor antagonism

Development of mechanical hypersensitivity in rats during heroin and ethanol dependence: Alleviation by CRF1 receptor antagonism

The amygdala, a relay station for switching on and off pain

Anti-inflammatory action of Justicia acuminatissima leaves

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