Reduction of arthritis and pain behaviour following chronic administration of amitriptyline or imipramine in rats with adjuvant-induced arthritis

Butler, Stephen; Weil-Fugazza, J.; Godefroy, F; Besson, Jean‐Marie

doi:10.1016/0304-3959(85)90057-0

Cited by 83 publications

(22 citation statements)

References 35 publications

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“…Thus, Neurotropin may alleviate hyperalgesia through the activation of descending pain inhibitory systems regardless of different pathogenesis of hyperalgesia. Amitriptyline and imipramine, monoamine re-uptake inhibitors, have also been shown to clearly reduce pain behavior in adjuvant-induced arthritic rats (37,38). These reports support that the activation of the descending pain inhibitory pathway is useful for relief of chronic pain.…”

Section: Discussionmentioning

confidence: 63%

Mechanisms of Analgesic Action of Neurotropin on Chronic Pain in Adjuvant-Induced Arthritic Rat: Roles of Descending Noradrenergic and Serotonergic Systems

et al. 2005

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Abstract. Neurotropin ® , a non-protein extract from the inflamed skin of rabbits inoculated with vaccinia virus, has been clinically used as an analgesic drug for treatment of chronic pain. In this study, we investigated the analgesic mechanisms of Neurotropin in the adjuvant-induced arthritic rat, a chronic pain model with inflammation. Neurotropin caused dose-dependent inhibition of hyperalgesia in the adjuvant-induced arthritic rat after single intravenous (10 -100 NU / kg) and oral (30 -200 NU / kg) administration. The analgesic effect of Neurotropin (intravenous 100 NU / kg and oral 200 NU/ kg) was significantly inhibited by intrathecal injections of the a 2 -adrenoceptor antagonist yohimbine (30 nmol / animal) and the selective 5-HT 3 serotonin receptor antagonist MDL72222 (30 nmol / animal), and slightly inhibited by the non-selective serotonin receptor antagonist methysergide (100 nmol / animal). The results suggest that the analgesic action of Neurotropin is at least in part due to the enhancement of noradrenergic and serotonergic descending pain inhibitory pathways. Neurotropin may be useful for the clinical management of chronic pain diseases such as a rheumatoid arthritis and osteoarthritis.

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Section: Discussionmentioning

confidence: 63%

Mechanisms of Analgesic Action of Neurotropin on Chronic Pain in Adjuvant-Induced Arthritic Rat: Roles of Descending Noradrenergic and Serotonergic Systems

et al. 2005

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“…There are few reports concerning the analgesic efficacy after single administration of antidepressants in the CFA-induced arthritic rats, although it has been reported that chronic (4 weeks) administration of amitriptyline or imipramine does not modify the mechanical threshold measured with the paw pressure test (Butler et al, 1985). When the survey is extended to other inflammatory pain models, it has been reported that intrathecal amitriptyline reverses thermal hyperalgesia measured with the plantar test in the carrageenan-induced inflamed rats (Eisenach and Gebhart, 1995).…”

mentioning

confidence: 99%

Allodynia and Hyperalgesia in Adjuvant-Induced Arthritic Rats: Time Course of Progression and Efficacy of Analgesics

Nagakura¹,

Okada²,

Kohara³

et al. 2003

J Pharmacol Exp Ther

161

140

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The complete Freund's adjuvant (CFA)-induced arthritic rat model has extensively served as a laboratory model in the study of arthritic pain. However, the time courses of allodynia and hyperalgesia and the efficacies of different analgesics have not fully been analyzed in this model. Mechanical allodynia, thermal and joint hyperalgesia, and other disease development parameters (body weight, mobility, paw volume, and joint stiffness) were measured on postinoculation days (PIDs) 0 to 28 in rats. Acute analgesic efficacies of drugs were evaluated on PID 9 when degrees of allodynia, hyperalgesia, and joint stiffness in the ipsilateral paw reached almost the maximum, although those in the contralateral paw changed only slightly. In the ipsilateral paw, thermal hyperalgesia reached the maximum on PID 1, whereas mechanical allodynia and joint hyperalgesia progressively developed during the first 7 or 8 days, being tuned in to arthritis development. In the contralateral paw, thermal hyperalgesia never occurred, whereas mechanical allodynia and joint hyperalgesia developed after PID 11. Morphine and tramadol had full efficacies for all the pain parameters tested at sedation-inducing doses. Indomethacin and diclofenac significantly but partially improved thermal and joint hyperalgesia. Amitriptyline significantly reduced thermal and joint hyperalgesia only at sedation-inducing dose. Acetaminophen, carbamazepine, and gabapentin had, at the most, very small efficacies. In conclusion, the present study provided integrated information about the time course of pain and other disease development parameters in the CFA-induced arthritic rats, and clarified acute efficacies of different categories of analgesics for the allodynia and hyperalgesia.The complete Freund's adjuvant (CFA)-induced arthritic rat model has extensively served as a laboratory model in the study of arthritic pain. Mechanical allodynia, thermal hyperalgesia and pain on joint movement (joint hyperalgesia), which are prominent features in arthritic pain, have proved to be present in it (Tatsuo et al., 1994;Jasmin et al., 1998;Bertorelli et al., 1999). The time courses of their progression after the CFA inoculation, however, have not been fully analyzed. The first aim in the present study, therefore, was to provide integrated information about the time courses of pain (mechanical allodynia, thermal hyperalgesia, and joint hyperalgesia) and other disease development (body weight, mobility, paw volume, and joint stiffness) parameters after the CFA inoculation into the single hind paw in rats. Surprisingly, there are no studies that have fully evaluated the analgesic efficacies of different categories of analgesics on mechanical allodynia, thermal hyperalgesia, and joint hyperalgesia in the CFA-induced arthritic rat model. The second aim in the present study, therefore, was to investigate this issue. Antipyretics (e.g., acetaminophen) and nonsteroidal anti-inflammatory drugs (e.g., indomethacin and diclofenac) are the first line drugs in the treatment of arth...

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“…The method to determine the numerical arthritis scores was similar to those described previously (3,21). Peripheral joints were measured with a caliper and were assigned a score between 0 (no swelling) and 4 (Ͼ40 and Ͼ70% increase in diameter of the ankle and wrist joints, respectively).…”

Section: Methodsmentioning

confidence: 99%

The vir Gene of Bacteriophage MAV1 Confers Resistance to Phage Infection on Mycoplasma arthritidis

Clapper¹,

Elgavish

et al. 2004

J Bacteriol

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Lysogenization of Mycoplasma arthritidis with the MAV1 bacteriophage increases the virulence of the mycoplasma in rats. The MAV1 vir gene is one of only two constitutively transcribed phage genes in the lysogen. We show here that Vir is a lipoprotein and is located on the outer surface of the cell membrane. To investigate whether Vir is a virulence factor, the vir gene was cloned into the transposon vector Tn4001T and inserted in the genome of the nonlysogen strain 158. The virulence of the resulting transformants was no different from that of the parent strain. Interestingly, all vir-containing transformants were resistant to infection by MAV1. Vir had no effect on MAV1 adsorption. We conclude that Vir is not a virulence factor but functions to exclude superinfecting phage, possibly by blocking the injection of phage DNA into the bacterial cytoplasm.Mycoplasmas are pathogens of humans and a variety of animals and plants (9). Among the members of the animal kingdom, primary sites of mycoplasmal infections are the membranes of the respiratory and urogenital tracts and joints (5). Mycoplasmas have some of the smallest genomes (as small as 0.58 Mb) in the prokaryotic kingdom (10). Consequently, their coding capacity is severely limited. The mycoplasmas lack a functional tricarboxylic acid cycle, a cytochrome-mediated electron transport chain system, and pathways for de novo biosynthesis of purines (9). They cannot synthesize cholesterol but require it for growth (6). Hence, mycoplasmas are dependent on their host for numerous nutrients and have a parasitic lifestyle.Mycoplasma arthritidis is a natural rat pathogen, but disease can be induced experimentally in both rats and mice by intravenous injection of bacteria (21). Rats typically present with acute polyarthritis lasting 6 to 8 weeks, whereas disease in mice is a chronic arthritis with periods of remission and exacerbation that can persist for the life of the animal (4). Few virulence factors have been identified in mycoplasmas in general and in M. arthritidis in particular. The immunomodulating factor MAM (5), a soluble T-cell mitogen, and adhesins such as MAA1 and MAA2 (23) have been suggested as possible M. arthritidis virulence factors, but correlation between these proteins and virulence has not been established conclusively. All strains of M. arthritidis are thought to produce MAM, but many MAM-producing strains are of low virulence (4). Like MAM, the cytadhesins are found in strains of both high and low virulence (20). Therefore, other factors influencing disease must exist.Unlike MAM and the MAA adhesins, the presence of MAV1 DNA in the bacterial chromosome strongly correlates with a virulent phenotype. In a previous study, the virulence of 20 M. arthritidis strains was examined (21). Ten of the strains were MAV1 lysogens and were highly virulent, whereas the other 10 strains were of low virulence and lacked the bacteriophage. For lysogenization, MAV1 DNA can insert into any of numerous sites in the mycoplasmal chromosome (17). A lowvirulence strain, 15...

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Reduction of arthritis and pain behaviour following chronic administration of amitriptyline or imipramine in rats with adjuvant-induced arthritis

Cited by 83 publications

References 35 publications

Mechanisms of Analgesic Action of Neurotropin on Chronic Pain in Adjuvant-Induced Arthritic Rat: Roles of Descending Noradrenergic and Serotonergic Systems

Mechanisms of Analgesic Action of Neurotropin on Chronic Pain in Adjuvant-Induced Arthritic Rat: Roles of Descending Noradrenergic and Serotonergic Systems

Allodynia and Hyperalgesia in Adjuvant-Induced Arthritic Rats: Time Course of Progression and Efficacy of Analgesics

The vir Gene of Bacteriophage MAV1 Confers Resistance to Phage Infection on Mycoplasma arthritidis

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