Differential stress effects on responses to noxious stimuli as measured by tail-flick latency and squeak threshold in rats

1987 ◽  
Vol 129 (3) ◽  
pp. 401-406 ◽  
Author(s):  
K. H. HUANG ◽  
B. C. SHYU
Keyword(s):  
Tail Flick ◽  
Differential Stress ◽  
Stress Effects ◽  
Tail Flick Latency ◽  
Noxious Stimuli

5-HT1A Receptors Mediate Analgesia Induced by Emulsified Sevoflurane in Thermal Nociception but Have Little Effect on Chemical Nociception

Pharmacology ◽  
2017 ◽  
Vol 100 (1-2) ◽  
pp. 25-30
Author(s):  
Chen Yan ◽  
Dai Ti-jun ◽  
Li Xin ◽  
Cao Gao ◽  
Jiang Shen ◽  
...  
Keyword(s):  
Analgesic Effect ◽  
Intraperitoneal Injection ◽  
Serotonin Receptor ◽  
Intrathecal Injection ◽  
Tail Flick ◽  
Hot Plate Test ◽  
Thermal Nociception ◽  
Tail Flick Latency ◽  
Specific Antagonist ◽  
The Relationship

Objective: The study aimed to investigate the relationship between the analgesic effect of sevoflurane and 5-serotonin receptor 1A (5-HT1A R) in the spinal cords of mice. Methods: Analgesic mouse models were established by intraperitoneal injection of emulsified sevoflurane, and the influence of p-MPPF (a specific antagonist of 5-HT1A Rs) intrathecal injection on the changes in tail-flick latency in tail-withdrawal test, pain threshold in hot-plate test (HPPT), and writhing times in acetic acid-induced writhing test were recorded. Results: Intraperitoneal injection of emulsified sevoflurane alone produced an analgesic effect (p < 0.05). p-MPPF (2, 4, and 8 μg) alone had no impact on tail-flick latency, HPPT, and writhing times in mice (p > 0.05). The 3 doses of p-MPPF reduced the tail-flick latency or HPPT. p-MPPF 8 μg can increase the writhing times (p < 0.05) in analgesic mice with sevoflurane, while p-MPPF 2 and 4 μg did not affect the writhing times. Conclusion: 5-HT1A Rs in the spinal cord may be an important target for the analgesic effect of sevoflurane on the thermal nociception, but it has little relation to the anti-chemical chemical nociceptive effect of sevoflurane.

Inhibition and facilitation of different nocifensor reflexes by spatially remote noxious stimuli

1994 ◽  
Vol 72 (3) ◽  
pp. 1152-1160 ◽  
Author(s):  
M. M. Morgan ◽  
M. M. Heinricher ◽  
H. L. Fields
Keyword(s):  
Conditioning Stimulus ◽  
Hot Water ◽  
Noxious Stimulus ◽  
Tail Flick ◽  
Withdrawal Reflex ◽  
Dorsal Horns ◽  
Electrophysiological Studies ◽  
Noxious Stimuli ◽  
Evoked Activity ◽  
Lumbar Spinal

1. Noxious stimuli have been shown to produce a diffuse inhibition of nociresponsive neurons in the spinal and trigeminal dorsal horns. The present study sought to extend these electrophysiological studies of diffuse noxious inhibitory controls (DNIC) by determining the effect of a spatially remote noxious stimulus on behavioral measures of nociception. Changes in latency for hindpaw withdrawal and tail flick reflexes were measured in lightly halothane-anesthetized or awake, spinally transected rats before, during, and after application of a spatially remote noxious stimulus. 2. Surprisingly, in no case did application of a spatially remote noxious stimulus inhibit the hindpaw withdrawal reflex. The latency for this reflex was either reduced or did not change when the tail or contralateral hindpaw was placed in hot water (50 degrees C) or when a noxious pinch was applied to the ear. In contrast, the latency for the tail flick reflex was consistently increased when the hindpaw was placed in hot water. Both the hindpaw reflex facilitation and the tail flick reflex inhibition produced by a noxious conditioning stimulus were attenuated in spinally transected rats indicating supraspinal modulation of both reflexes. 3. In addition, and consistent with the work of others, placing the tail in hot water reduced the evoked activity of convergent neurons in both the trigeminal and lumbar spinal dorsal horns. Thus inhibition of the activity of nociresponsive neurons in the dorsal horn is consistent with inhibition of the tail flick reflex, but not with facilitation of the hindpaw withdrawal reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Low Concentrations of Halothane Increase Response to a Noxious Thermal Stimulus and Attenuate the Antinociceptive Effect of Intraventricular but Not Intrathecal Morphine

2001 ◽  
Vol 94 (2) ◽  
pp. 298-302 ◽  
Author(s):  
Kenneth Drasner
Keyword(s):  
Pain Perception ◽  
Intrathecal Morphine ◽  
Antinociceptive Effect ◽  
Maximum Effect ◽  
Tail Flick ◽  
Temperature Threshold ◽  
Thermal Stimulus ◽  
Descending Inhibition ◽  
Low Concentrations ◽  
Tail Flick Latency

Background Classically, the first plane of anesthesia is known as the stage of analgesia. Nonetheless, clinical evidence suggests that low doses of inhaled agents might enhance pain perception. The present experiments test the hypothesis that low concentrations of halothane increase response to a noxious thermal stimulus and attenuate the antinociceptive effect of intraventricular morphine via disruption of descending inhibition. Methods In the first experiment, the temperature at which rats withdraw their tails from a heat source was measured in animals breathing various concentrations of halothane. In the second experiment, the effect of intraventricular or intrathecal morphine on tail-flick latency was assessed in rats breathing either oxygen or 0.23% halothane. Results Low concentrations of halothane decreased the temperature threshold for tail-flick with a maximum effect at 0.06% atmospheres. Halothane attenuated the antinociceptive potency of intraventricular morphine but enhanced the efficacy of intrathecal morphine. Conclusions Subanesthetic concentrations of halothane may enhance response to a noxious stimulus. The differential effect on intraventricular and intrathecal morphine suggests that this enhancement results from disruption of descending inhibition.

Dexmedetomidine Enhances Analgesic Action of Nitrous Oxide

2004 ◽  
Vol 100 (4) ◽  
pp. 894-904 ◽  
Author(s):  
Cecilia Dawson ◽  
Daqing Ma ◽  
Andre Chow ◽  
Mervyn Maze
Keyword(s):  
Spinal Cord ◽  
Nitrous Oxide ◽  
Neuronal Activity ◽  
Locus Ceruleus ◽  
Tail Flick ◽  
Receptor Subtypes ◽  
Dental Surgery ◽  
Analgesic Effects ◽  
Adrenoceptor Antagonist ◽  
Tail Flick Latency

Background Nitrous oxide and dexmedetomidine are thought to mediate analgesia (antinociception in a noncommunicative organism) via alpha 2B- and alpha 2A-adrenergic receptor subtypes within the spinal cord, respectively. Nitrous oxide and dexmedetomidine exert diametrically opposite effects on neuronal activity within the locus ceruleus, a pivotal site for modulation of analgesia. Because of these differences, the authors explored whether the two analgesics in combination would provide satisfactory analgesia. Methods The analgesic effects of nitrous oxide and dexmedetomidine given both intraperitoneally and intrathecally were evaluated using the tail-flick latency test in rats. For investigation of the interaction, rats were pretreated with dexmedetomidine, either intraperitoneally or intrathecally, immediately before nitrous oxide exposure such that peak antinociceptive effects of each drug coincided. For assessment of the effect on tolerance, dexmedetomidine was administered as tolerance to nitrous oxide developed. Expression of c-Fos was used to assess neuronal activity in the locus ceruleus. Results Nitrous oxide and dexmedetomidine increased tail-flick latency with an ED50 (mean +/- SEM) of 55.0 +/- 2.2% atm for nitrous oxide, 27.6 +/- 5.1 for microg/kg intraperitoneal dexmedetomidine, and 2.9 +/- 0.1 microg for intrathecal dexmedetomidine. Combinations of systemically administered dexmedetomidine and nitrous oxide produced an additive analgesic interaction; however, neuraxially administered dexmedetomidine interacted synergistically with nitrous oxide. Tolerance to nitrous oxide was reversed by coadministration of dexmedetomidine. Prazosin, the alpha 1-/alpha 2B-adrenoceptor antagonist, attenuated the analgesic effect of nitrous oxide and prevented dexmedetomidine-induced reversal of tolerance to nitrous oxide. Nitrous oxide-induced increase of neuronal activity in the locus ceruleus was reversed by dexmedetomidine. Conclusion The synergistic analgesic interaction between nitrous oxide and dexmedetomidine within the spinal cord is obscured by a supraspinal antagonism when dexmedetomidine is administered systemically in the pretolerant state. After tolerance to nitrous oxide develops, supraspinal functional antagonism no longer obtains exposing the synergistic action at the level of the spinal cord, which expresses itself as a reversal of the tolerant state. The authors speculate that the addition of dexmedetomidine to nitrous oxide is likely to provide enhanced and more durable analgesia in settings in which nitrous oxide is currently used alone (e.g., labor and dental surgery).

scholarly journals Effect of Rosmarinic and Caffeic Acids on Inflammatory and Nociception Process in Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Giovana Duzzo Gamaro ◽  
Edna Suyenaga ◽  
Milene Borsoi ◽  
Joice Lermen ◽  
Patrícia Pereira ◽  
...  
Keyword(s):  
Caffeic Acid ◽  
Rosmarinic Acid ◽  
Pleural Cavity ◽  
Biological Activities ◽  
Control Group ◽  
Tail Flick ◽  
Nociceptive Response ◽  
Tail Flick Latency ◽  
Balanced Distribution ◽  
Anti Inflammatory

Rosmarinic acid is commonly found in species of the Boraginaceae and the subfamily Nepetoideae (Lamiaceae). It has a number of interesting biological activities, for example, antiviral, antibacterial, anti-inflammatory, and antioxidant. The aim of the present study was to investigate the effect of the i.p. administration of caffeic and rosmarinic acid (5 and 10 mg/kg) on anti-inflammatory and nociceptive response using carrageenan-induced pleurisy model and tail-flick assay in rats. The analysis of cells in the pleural exudates revealed a reduction of 66% of the number of leukocytes that migrated to the pleural cavity in the animals treated with 5 mg/kg caffeic acid, and of 92.9% for the animals treated with 10 mg/kg in comparison with the control group. These exudates showed a balanced distribution of polymorphonuclear (PMN) and mononuclear (MN) cells, differently from the control group, in which PMN cells were predominant. The analysis to tail-flick latency was increased in the group treated with 10 mg/kg caffeic acid characterizing a nociceptive response. While there was no difference between control group and animals treated with rosmarinic.

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