Evidence for an exclusive antinociceptive effect of nociceptin/orphanin FQ, an endogenous ligand for the ORL1 receptor, in two animal models of neuropathic pain

Pain ◽  
2004 ◽  
Vol 110 (1) ◽  
pp. 236-245 ◽  
Author(s):  
Christine Courteix ◽  
Marie-Ange Coudoré-Civiale ◽  
Anne-Marie Privat ◽  
Teresa Pélissier ◽  
Alain Eschalier ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Animal Models ◽  
Antinociceptive Effect ◽  
Orphanin Fq ◽  
Endogenous Ligand ◽  
Orl1 Receptor

Nociceptin, a novel endogenous ligand for the ORL1 receptor, has potent erectile activity in the cat

1997 ◽  
Vol 273 (1) ◽  
pp. E214-E219 ◽  
Author(s):  
H. C. Champion ◽  
R. Wang ◽  
W. J. Hellstrom ◽  
P. J. Kadowitz
Keyword(s):  
Drug Combination ◽  
Nitric Oxide Donor ◽  
The Novel ◽  
Orphanin Fq ◽  
Endogenous Ligand ◽  
Intracavernosal Injection ◽  
Orl1 Receptor ◽  
Arterial Blood ◽  
Intracavernosal Injections ◽  
G Protein Coupled

The heptadecapeptide nociceptin, also known as orphanin FQ, is a newly discovered endogenous ligand for the opioid-like G protein-coupled receptor ORL1. The present study was undertaken to investigate the effects of intracavernosal injections of nociceptin on penile erection in anesthetized cats. Responses to nociception were compared with erectile responses elicited by intracavernosal injection of vasoactive intestinal polypeptide (VIP), adrenomedullin (ADM), the novel nitric oxide donor diethylaminenitric oxide complex sodium (DEA/NO), and the control triple-drug combination (papaverine, phentolamine, and prostaglandin E1). The order of potency was VIP > ADM > nociceptin > DEA/NO. Intracavernosal injections of nociceptin in doses of 0.3-30 nmol elicited dose-related increases in cavernosal pressure and penile length that were comparable to those induced by the triple-drug combination, which is used in the treatment of erectile dysfunction. The response to nociceptin was rapid in onset, and the duration of the peak pressure increase and total response was significantly shorter than the response to the control triple-drug combination but longer in duration than responses to VIP and ADM. Intracavernosal injection of the triple-drug combination resulted in a greater decrease in mean systemic arterial blood pressure than did nociceptin. These data demonstrate that intracavernosal injection of this novel endogenous ligand for the ORL1 receptor induces a potent and relatively long-lasting erectile response in the cat.

Antinociceptive effect of Brazilian armed spider venom toxin Tx3–3 in animal models of neuropathic pain

Pain ◽  
2011 ◽  
Vol 152 (10) ◽  
pp. 2224-2232 ◽  
Author(s):  
Gerusa Duarte Dalmolin ◽  
Cássia Regina Silva ◽  
Flávia Karine Rigo ◽  
Guilherme Monteiro Gomes ◽  
Marta do Nascimento Cordeiro ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Animal Models ◽  
Antinociceptive Effect ◽  
Spider Venom ◽  
Venom Toxin

scholarly journals The activation of galanin receptor 2 plays an antinociceptive effect in nucleus accumbens of rats with neuropathic pain

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Yan Dong ◽  
Chong-Yang Li ◽  
Xiao-Min Zhang ◽  
Ya-Nan Liu ◽  
Shuang Yang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Nucleus Accumbens ◽  
Pain Threshold ◽  
Antinociceptive Effect ◽  
Galanin Receptor ◽  
Pain Model ◽  
Withdrawal Threshold ◽  
Neuropathic Pain Model ◽  
Galanin Receptors ◽  
Intact Rats

AbstractOur previous research has shown that galanin plays an antinociceptive effect via binding to galanin receptors (GalRs) in nucleus accumbens (NAc). This study focused on the involvement of GalR2 in galanin-induced antinociceptive effect in NAc of neuropathic pain rats. The chronic constriction injury of sciatic nerve (CCI) was used to mimic neuropathic pain model. The hind paw withdrawal latency (HWL) to thermal stimulation and hind paw withdrawal threshold (HWT) to mechanical stimulation were measured as the indicators of pain threshold. The results showed that 14 and 28 days after CCI, the expression of GalR2 was up-regulated in bilateral NAc of rats, and intra-NAc injection of GalR2 antagonist M871 reversed galanin-induced increases in HWL and HWT of CCI rats. Furthermore, intra-NAc injection of GalR2 agonist M1145 induced increases in HWL and HWT at day 14 and day 28 after CCI, which could also be reversed by M871. Finally, we found that M1145-induced antinociceptive effect in NAc of CCI rats was stronger than that in intact rats. These results imply that the GalR2 is activated in the NAc from day 14 to day 28 after CCI and GalR2 is involved in the galanin-induced antinociceptive effect in NAc of CCI rats.

NMDA Antagonist Peptide Supplementation Enhances Pain Alleviation by Adrenal Medullary Transplants

2005 ◽  
Vol 14 (4) ◽  
pp. 203-211 ◽  
Author(s):  
Farinaz Nasirinezhad ◽  
Jacqueline Sagen
Keyword(s):  
Neuropathic Pain ◽  
Animal Models ◽  
Striated Muscle ◽  
Thermal Hyperalgesia ◽  
Nmda Antagonist ◽  
Nmda Receptor Antagonist ◽  
Intraplantar Injection ◽  
Amino Acid Peptide ◽  
Spinal Subarachnoid Space ◽  
Pain Symptoms

Spinal transplantation of adrenal medullary chromaffin cells has been shown to decrease pain responses in several animal models. Improved potency may be possible by engineering cells to produce greater levels of naturally derived analgesics. As an initial screen for potential candidates, adrenal medullary transplants were evaluated in combination with exogenously administered neuropeptides in rodent pain models. Histogranin is a 15-amino acid peptide that exhibits NMDA receptor antagonist activity. The stable derivative [Ser1]histogranin (SHG) can attenuate pain symptoms in some animal models. The formalin model for neurogenic inflammatory pain and the chronic constriction injury (CCI) model for neuropathic pain were used to evaluate the combined effects of chromaffin cell transplantation and intrathecal (IT) SHG injections. Animals were implanted with either adrenal medullary or control striated muscle tissue in the spinal subarachnoid space. For evaluation of formalin responses, animals were pretreated with SHG (0.5, 1.0, 3.0 μg) followed by an intraplantar injection of formalin, and flinching responses were quantified. Pretreatment with SHG had no significant effect on flinching behavior in control animals at lower doses, with incomplete attenuation only at the highest dose. In contrast, 0.5 μg SHG significantly reduced flinching responses in animals with adrenal medullary transplants, and 1.0 μg nearly completely eliminated flinching in these animals in the tonic phase. For evaluation of effects on neuropathic pain, animals received transplants 1 week following CCI, and were tested for thermal and mechanical hyperalgesia and cold allodynia before and following SHG treatment. The addition of low doses of SHG nearly completely eliminated neuropathic pain symptoms in adrenal medullary transplanted animals, while in control transplanted animals only thermal hyperalgesia was attenuated, at the highest dose of SHG. These results suggest that SHG can augment adrenal medullary transplants, and the combination may result in improved effectiveness and range in the treatment of chronic pain syndromes.

The role of brain-derived neurotrophic factor in different animal models of neuropathic pain

2010 ◽  
Vol 14 (5) ◽  
pp. 473.e1-473.e9 ◽  
Author(s):  
Pascal Vanelderen ◽  
Tom Rouwette ◽  
Tamas Kozicz ◽  
Eric Roubos ◽  
Jan Van Zundert ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Animal Models ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor

Neuropathic pain models in the development of analgesic drugs

2011 ◽  
Vol 2 (4) ◽  
pp. 172-177 ◽  
Author(s):  
Per Hartvig Honoré ◽  
Anna Basnet ◽  
Laila Eljaja ◽  
Pernille Kristensen ◽  
Lene Munkholm Andersen ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Animal Models ◽  
Nerve Injury ◽  
Clinical Manifestations ◽  
Pharmacological Intervention ◽  
Special Focus ◽  
Surgical Performance ◽  
Neuropathic Pain Syndrome ◽  
Pain Models ◽  
Rats And Mice

AbstractIntroductionAnimal disease models are predictive for signs seen in disease. They may rarely mimic all signs in a specific disease in humans with respect to etiology, cause or development. Several models have been developed for different pain states and the alteration of behavior has been interpreted as a response to external stimulus or expression of pain or discomfort. Considerable attention must be paid not to interpret other effects such as somnolence or motor impairment as a pain response and similarly not to misinterpret the response of analgesics.Neuropathic pain is caused by injury or disease of the somatosensory system. The clinical manifestations of neuropathic pain vary including both stimulus-evoked and non-stimulus evoked (spontaneous) symptoms. By pharmacological intervention, the threshold for allodynia and hyperalgesia in the various pain modalities can be modulated and measured in animals and humans. Animal models have been found most valuable in studies on neuropathic pain and its treatment.Aim of the studyWith these interpretation problems in mind, the present text aims to describe the most frequently used animal models of neuropathic pain induced by mechanical nerve injury.MethodsThe technical surgical performance of these models is described as well as pain behavior based on the authors own experience and from a literature survey.ResultsNerve injury in the hind limb of rats and mice is frequently used in neuropathic pain models and the different types of lesion may afford difference in the spread and quality of the pain provoked. The most frequently used models are presented, with special focus on the spared nerve injury (SNI) and the spinal nerve ligation/transection (SNL/SNT) models, which are extensively used and validated in rats and mice. Measures of mechanical and thermal hypersensitivity with von Frey filaments and Hargreaves test, respectively, are described and shown in figures.ConclusionsA number of animal models have been developed and described for neuropathic pain showing predictive value in parallel for both humans and animals. On the other hand, there are still large knowledge gaps in the pathophysiologic mechanisms for the development, maintenance and progression of the neuropathic pain syndromeImplicationsBetter understanding of pathogenic mechanisms of neuropathic pain in animal models may support the search for new treatment paradigms in patients with complex neuropathic pain conditions

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