Nitrous Oxide Lacks the Antinociceptive Effect on the Tail Flick Test in Newborn Rats

2000 ◽  
Vol 91 (1) ◽  
pp. 6-10 ◽  
Author(s):  
Masahiko Fujinaga ◽  
Ryan Doone ◽  
M. Frances Davies ◽  
Mervyn Maze
Keyword(s):  
Nitrous Oxide ◽  
Antinociceptive Effect ◽  
Tail Flick ◽  
Newborn Rats ◽  
Tail Flick Test

Nitrous Oxide Lacks the Antinociceptive Effect on the Tail Flick Test in Newborn Rats

2000 ◽  
Vol 91 (1) ◽  
pp. 6-10
Author(s):  
Masahiko Fujinaga ◽  
Ryan Doone ◽  
M. Frances Davies ◽  
Mervyn Maze
Keyword(s):  
Nitrous Oxide ◽  
Antinociceptive Effect ◽  
Tail Flick ◽  
Newborn Rats ◽  
Tail Flick Test

scholarly journals Effects of peripheral FAAH blockade on NTG-induced hyperalgesia—evaluation of URB937 in an animal model of migraine

Cephalalgia ◽  
2015 ◽  
Vol 35 (12) ◽  
pp. 1065-1076 ◽  
Author(s):  
R Greco ◽  
T Bandiera ◽  
AS Mangione ◽  
C Demartini ◽  
F Siani ◽  
...  
Keyword(s):  
Animal Model ◽  
Antinociceptive Effect ◽  
Acid Amide ◽  
Male Rats ◽  
Tail Flick ◽  
Tail Flick Test ◽  
Brain Nuclei ◽  
Nociceptive Responses ◽  
Fos Expression ◽  
Baseline Conditions

Background Systemic nitroglycerin (NTG) activates brain nuclei involved in nociceptive transmission as well as in neuroendocrine and autonomic functions in rats. These changes are considered relevant for migraine because NTG consistently provokes spontaneous-like migraine attacks in migraineurs. Several studies have suggested a relationship between the endocannabinoid levels and pain mediation in migraine. URB937, a peripheral inhibitor of fatty acid amide hydrolase (FAAH)—the enzyme that degrades anandamide, produces analgesia in animal models of pain, but there is no information on its effects in migraine. Aim We evaluated whether URB937 alters nociceptive responses in the animal model of migraine based on NTG administration in male rats, using the tail flick test and the plantar and orofacial formalin tests, under baseline conditions and after NTG administration. Furthermore, we investigated whether URB937 affects NTG-induced c-Fos expression in the brain. Results During the tail flick test, URB937 showed an antinociceptive effect in baseline conditions and it blocked NTG-induced hyperalgesia. URB937 also proved effective in counteracting NTG-induced hyperalgesia during both the plantar and orofacial formalin tests. Mapping of brain nuclei activated by NTG indicates that URB937 significantly reduces c-Fos expression in the nucleus trigeminalis caudalis and the locus coeruleus. Conclusions The data suggest that URB937 is capable of changing, probably via indirect mechanisms, the functional status of central structures that are important for pain transmission in an animal model of migraine.

Antinociceptive Profiles of Platycodin D in the Mouse

2004 ◽  
Vol 32 (02) ◽  
pp. 257-268 ◽  
Author(s):  
Seong-Soo Choi ◽  
Eun-Jung Han ◽  
Tae-Hee Lee ◽  
Ki-Jung Han ◽  
Han-Kyu Lee ◽  
...  
Keyword(s):  
Antinociceptive Effect ◽  
Control Level ◽  
Tail Flick ◽  
Triterpene Saponins ◽  
Tail Flick Test ◽  
Platycodin D ◽  
Pain Models ◽  
Antinociceptive Effects ◽  
Dose Dependent ◽  
Higher Doses

Platycodin D (PD), one of several triterpene saponins, was isolated from roots of Platycodon grandiflorum. We previously reported that intracerebroventricular (i.c.v.) administration of PD showed an antinociceptive effect as measured by the tail-flick assay. However, its exact role in the regulation of antinociception in the various types of pain models has not yet been characterized. Thus, we attempted to find antinociceptive profiles of PD in various pain models. PD administered intraperitoneally (i.p.), i.c.v. or intrathecally (i.t.) showed antinociceptive effects in dose-dependent manners as measured by the tail-flick, writhing and formalin tests. In the tail-flick test, PD at the low doses reached the peak after 15 minutes and returned to the control level after 60 minutes. However, higher doses of PD showed a strong antinociception at least for 1 hour. PD administered i.t. showed stronger antinociception than that induced by i.c.v. administration PD in both tail-flick and writhing tests. In the formalin test, PD administered i.p., i.c.v. or i.t. showed antinociceptive effects during both the first (direct nociceptive stimulation) and second (late inflammatory) phases. Pretreatment with naltrexone i.p., i.c.v. or i.t. did not affect PD-induced inhibition of the tail-flick response. Our results suggest that PD shows a strong antinociceptive effect on the tail-flick, writhing and formalin tests, acting on central nervous system. However, PD-induced antinociception may not be mediated by the opioid receptors.

Nitrous Oxide Produces Antinociceptive Response via α2Band/or α2CAdrenoceptor Subtypes in Mice 

1999 ◽  
Vol 90 (2) ◽  
pp. 470-476 ◽  
Author(s):  
Tian-Zhi Guo ◽  
Frances M. Davies ◽  
Wade S. Kingery ◽  
Andrew J. Patterson ◽  
Lee E. Limbird ◽  
...  
Keyword(s):  
Nitrous Oxide ◽  
Transgenic Mice ◽  
Time Course ◽  
Antinociceptive Effect ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Tail Flick ◽  
Wild Type ◽  
Tail Flick Latency ◽  
In The Wild

Background Opiate receptors in the periaqueductal gray region and alpha2 adrenoceptors in the spinal cord of the rat mediate the antinociceptive properties of nitrous oxide (N2O). The availability of genetically altered mice facilitates the detection of the precise protein species involved in the transduction pathway. In this study, the authors establish the similarity between rats and mice in the antinociceptive action of N2O and investigate which alpha2 adrenoceptor subtypes mediate this response. Methods After obtaining institutional approval, antinociceptive dose-response and time-course to N2O was measured in wild-type and transgenic mice (D79N), with a nonfunctional alpha2A adrenoceptor using tail-flick latency. The antinociceptive effect of N2O was tested after pretreatment systemically with yohimbine (nonselective alpha2 antagonist), naloxone (opiate antagonist), L659,066 (peripheral alpha2-antagonist) and prazosin (alpha2B- and alpha2C-selective antagonist). The tail-flick latency to dexmedetomidine (D-med), a nonselective alpha2 agonist, was tested in wild-type and transgenic mice. Results N2O produced antinociception in both D79N transgenic and wild-type litter mates, although the response was less pronounced in the transgenic mice. Antinociception from N2O decreased over time with continuing exposure, and the decrement was more pronounced in the transgenic mice. The antinociceptive response could be dose dependently antagonized by opiate receptor and selective alpha2B-/alpha2C-receptor antagonists but not by a central nervous system-impermeant alpha2 antagonist (L659,066). Whereas dexmedetomidine exhibited no antinociceptive response in the D79N mice, the robust antinociceptive response in the wild-type litter mates could not be blocked by a selective alpha2B-/alpha2C-receptor antagonist. Conclusion These data confirm that the antinociceptive response to an exogenous alpha2-agonist is mediated by an alpha2A adrenoceptor and that there appears to be a role for the alpha2B- or alpha2C-adrenoceptor subtypes, or both, in the analgesic response to N2O.

scholarly journals Heparin sensitization of fentanyl initiated mu-receptors

2021 ◽  
pp. 20-32
Author(s):  
А.Е. Khomutov ◽  
◽  
А.V. Deryugina ◽  
А.S. Lizunova ◽  
Z.V. Bobrova ◽  
...  
Keyword(s):  
Opioid Receptors ◽  
Anticoagulant Activity ◽  
Antinociceptive Effect ◽  
Regulatory Peptides ◽  
Tail Flick ◽  
Mu Opioid Receptors ◽  
Opioid Agonist ◽  
Hypotensive Action ◽  
Tail Flick Test ◽  
Mu Opioid

Heparin is an anticoagulant widely used in clinical practice. In addition to anticoagulant activity, heparin has a cytostatic, bacteriostatic, antilipemic, radioprotective effect, and exhibits antiallergic and hypotensive action. Heparin modulates cardiotropic, neurotropic, antihypoxic, anti-ischemic properties of regulatory peptides and pharmacological agents used in pain relief and anesthesia. At the same time, there is very little information about the antinociceptive effect of heparin. The aim of this work is to study the effect of heparin in combination with the opioid agonist fentanyl on mu-opioid receptors at the spinal and supraspinal levels. In experiments on laboratory rats, it was established that heparin, when pre-administered and combined with fentanyl, increases the latency in the tail flick test and the paw licking test. Naloxone, an opioid receptor antagonist, reduces antinociceptive efficacy of the studied compounds. Protamine sulfate also reduces the level of heparin sensitization of opioid receptors. Thus, the obtained data allow us to speak about the sensitizing effect of heparin on initiated by an agonist mu-opioid receptors at the spinal and supraspinal levels.

scholarly journals Modulation of Morphine-induced Antinociception in Acute and Chronic Opioid Treatment by Ibudilast

2009 ◽  
Vol 111 (6) ◽  
pp. 1356-1364 ◽  
Author(s):  
Tuomas O. Lilius ◽  
Pekka V. Rauhala ◽  
Oleg Kambur ◽  
Eija A. Kalso
Keyword(s):  
Cell Activation ◽  
Antinociceptive Effect ◽  
Opioid Analgesics ◽  
Morphine Tolerance ◽  
Tail Flick ◽  
Sprague Dawley ◽  
Tail Flick Test ◽  
Glial Cell Activation ◽  
Sprague Dawley Rats ◽  
Antinociceptive Effects

Background Opioid analgesics are effective in relieving chronic pain, but they have serious adverse effects, including development of tolerance and dependence. Ibudilast, an inhibitor of glial activation and cyclic nucleotide phosphodiesterases, has shown potential in the treatment of neuropathic pain and opioid withdrawal. Because glial cell activation could also be involved in the development of opioid tolerance in rats, the authors studied the antinociceptive effects of ibudilast and morphine in different models of coadministration. Methods Antinociception was assessed using male Sprague- Dawley rats in hot plate and tail-flick tests. The effects of ibudilast on acute morphine-induced antinociception, induction of morphine tolerance, and established morphine tolerance were studied. Results Systemic ibudilast produced modest dose-related antinociception and decreased locomotor activity at the studied doses of 2.5-22.5 mg/kg. The highest tested dose of 22.5 mg/kg produced 52% of the maximum possible effect in the tail-flick test. It had an additive antinociceptive effect when combined with systemic morphine. Coadministration of ibudilast with morphine did not attenuate the development of morphine tolerance. However, in morphine-tolerant rats, ibudilast partly restored morphine-induced antinociception. Conclusions Ibudilast produces modest antinociception, and it is effective in restoring but not in preventing morphine tolerance. The mechanisms of the effects of ibudilast should be better understood before it is considered for clinical use.

scholarly journals Experimental study of analgesic mechanisms of 4-methyl-2,2-dioxo-1H-2λ6,1-benzothiazine-3-carboxylic acid derivative (compound NI-9) in rat

2021 ◽  
Vol 25 (1) ◽  
pp. 12-16
Author(s):  
О. V. Malchenko ◽  
N. І. Voloshchuk ◽  
O. V. Hrymalovska
Keyword(s):  
Carboxylic Acid ◽  
Antinociceptive Effect ◽  
Statistical Processing ◽  
Pain Syndrome ◽  
Modern Medicine ◽  
Mean Value ◽  
Tail Flick ◽  
Tail Flick Test ◽  
Pain Syndromes ◽  
The Mean

Annotation. The problem of effective and safe treatment of pain syndromes is a priority area of modern medicine, since pain syndrome is often accompanied by economic costs, a drop in labor productivity and an increase in the risk of other diseases. The derivative 4-methyl-2,2-dioxo-1H-2λ6,1-benzothiazine-3-carboxamide (compound NI-9) has shown a significant analgesic effect in various models of pain syndromes. The aim of this work was to experimentally study the mechanisms of the analgesic activity of compound NI-9 using pharmacological analyzers in the tail-flick test. The study was performed on 210 male Wistar rats. Statistical processing of the obtained results was performed using the software package STATISTICA 10.0 with the calculation of the mean value, standard error of the mean, confidence interval (p). The experiments used: naloxone, prazosin, clonidine, yohimbine, isoproterenol, propranolol, nalbuphine, chlorpromazine, dopamine, nakom, memantine, phenylephrine. The results showed that the opioidergic system was not involved in the antinociceptive effect of compound NI-9. At the same time, the participation of alpha-1 and alpha-2 adrenergic receptors, dopamine receptors, and also partially NMDA receptors has been proven. The data obtained serve as the basis for further preclinical studies of N- (4-methoxybenzyl) -4-methyl-2,2-dixo-1H-2Λ6,1-benzothiazine-3-carboxylic acid (compounds NI-9) as a non-narcotic analgesic, which can compete with already known drugs of this class in the treatment of diseases accompanied by inflammatory and pain syndrome.

scholarly journals The Effects of Ketamine and Its Enantiomers on the Morphine- or Dexmedetomidine-induced Antinociception after Intrathecal Administration in Rats

2000 ◽  
Vol 93 (1) ◽  
pp. 231-241 ◽  
Author(s):  
Gabriella Joó ◽  
Gyöngyi Horvath ◽  
Walter Klimscha ◽  
Gabriella Kekesi ◽  
Ildiko Dobos ◽  
...  
Keyword(s):  
Time Course ◽  
Antinociceptive Effect ◽  
Motor Impairment ◽  
Intrathecal Administration ◽  
Fixed Dose ◽  
Tail Flick ◽  
Tail Flick Test ◽  
Male Wistar Rats ◽  
Racemic Ketamine ◽  
Alpha2 Adrenoceptor

Background The spinal administration of some N-methyl-d-aspartate receptor antagonists results in antinociception and potentiates the effects of opioids and alpha2-adrenoceptor agonists, but ketamine and its enantiomers have not been examined. The present study investigated the interactions of racemic ketamine, R(-)-ketamine and S(+)-ketamine with morphine and with dexmedetomidine. Methods Intrathecal catheters were implanted into male Wistar rats. Three days later, the acute nociceptive sensitivity was assessed using the tail-flick test. Analgesic latencies were converted to the percentage maximum possible effect. The dose that yielded 50% of the maximum possible effect (ED50) and dose-response and time-course curves were determined for the ketamines (30-300 microg), morphine (0.1-3.0 microg), dexmedetomidine (0.3-10.0 microg), and mixtures of two doses of ketamines (30 or 100 microg) with different doses of morphine or dexmedetomidine for fixed-dose analysis. Results Neither racemic ketamine nor its enantiomers alone had a significant effect on the tail-flick test, with the exception of the highest dose of racemic ketamine, which caused motor impairment. Morphine and dexmedetomidine each produced dose-dependent antinociception, with ED50 of 1.7 microg (95% confidence interval: 1.04-2.32) and 4. 85 microg (3.96-5.79), respectively. A low dose (30 microg) of racemic ketamine or its enantiomers did not influence the ED50 of morphine significantly. Coadministration of 100 microg racemic ketamine or S(+)-ketamine, but not R(-)-ketamine, significantly enhanced and prolonged the antinociceptive effect of morphine. Both doses of racemic ketamine or its isomers significantly decreased the ED50 value for dexmedetomidine, although the higher dose of racemic or S(+)-ketamine had the highest potency. One-hundred micrograms of racemic ketamine or S(+)-ketamine also prolonged the effects of dexmedetomidine. Conclusions These data indicate that racemic ketamine and S(+)-ketamine, but not R(-)-ketamine, exhibit similar effectiveness in potentiating the antinociceptive effects of both morphine and dexmedetomidine.

Sign in / Sign up

Export Citation Format

Share Document