Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has recently been reported that male mice exhibit pronounced analgesia in response to attack from aggressive conspecifics. Although several studies indicate that this reaction can be blocked by opiate antagonist pretreatment, unequivocal evidence of opioid involvement is very much more limited. In the present study, the phenomenon of conflict analgesia has been studied in male DBA/2 intruder mice following exposure to a criterion level of attack from aggressive BKW residents. Our findings indicate that this analgesia is blocked and reversed by naloxone unaltered by methyl naloxone, except at high doses (75 mg/kg) and fully cross-tolerant with morphine. This profile confirms and extends earlier findings with B6AF1 mice, indicating that the opioid mediation of this biologically-relevant form of environmental analgesia is not strain specific.
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PMID:Social conflict analgesia: studies on naloxone antagonism and morphine cross-tolerance in male DBA/2 mice. 241 63

The relationship between analgesia and behavior during and after an aggressive encounter was investigated in saline- and opiate antagonist-treated DBA mice. A low number of bites induced an analgesia that was reversed by beta-chlornaltrexamine but not by naloxone, and that correlated positively with increased displays of defensive upright and immobility upon contact with the opponent. Extended attacks induced a naloxone-sensitive analgesia that was linked to a delayed occurrence of "panic" escape behavior. In the post-conflict phase, the degree of immobility and analgesia correlated positively in attacked mice. Naltrexone prevented this analgesia and lowered immobility. Endogenous opioids released during social conflict may induce analgesia and immobility in DBA mice.
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PMID:Relationship between behavioral and nociceptive changes in attacked mice: effects of opiate antagonists. 249 22

Recent studies have suggested that anxiety may be an important factor in the non-opioid analgesic response to defeat in muroid rodents. In the present study, we have examined the influence of the 5-HT1A receptor agonist, 8-OH-DPAT, on basal nociception and defeat analgesia in male DBA/2 mice. Our results show that, while devoid of intrinsic activity on the mouse tail-flick assay, 8-OH-DPAT blocks the analgetic consequences of defeat. A ten-fold potency differential was observed as a function of route of injection, with minimum effective doses of 0.1 and 1.0 mg/kg for subcutaneous and intraperitoneal administration, respectively. Although further studies are required, these preliminary data support 5-HT1A receptor involvement in the mediation of this form of adaptive pain inhibition.
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PMID:5HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), inhibits non-opioid analgesia in defeated mice: influence of route of administration. 252 55

The present paper describes the development and application of an enzyme-linked immunosorbent assay (ELISA) for the assessment of beta-endorphin-like immunoreactivity (beta-ELIR) level in the hypothalamus, the periaqueductal grey (PAG) and the pituitary of DBA/2 mice that were subjected to mild social stress (aggressive confrontation). After confrontation these subjects showed elevated tail-flick latencies (TFL) when compared to controls, a finding that indicates stress-induced analgesia (SIA). A positive correlation was found between individual TFLs and beta-ELIR levels in the PAG but not in the hypothalamus and the pituitary. These results suggest that individual baseline PAG beta-ELIR levels may be taken as a predictor of high degrees of stress-induced analgesia.
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PMID:Beta-endorphin-like immunoreactivity levels in the hypothalamus, the periaqueductal grey and the pituitary of the DBA mouse: determination by ELISA and relationship to nociception. 253 Jun

Acetorphan, a parenterally active enkephalinase inhibitor, induced dose-dependently a naloxone-reversible analgesia on the hot-plate jump test in DBA/2J (DBA2) mice but was devoid of effects in C57BL/6J (C57) mice. By contrast, acetorphan increased locomotion in both strains; however, the DBA2 strain was much more sensitive than C57 mice to the locomotor stimulant effect. The increased locomotion was antagonized by naloxone in both strains. These data suggest that endogenous enkephalins modulate nociception and locomotion in the two inbred strains differently.
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PMID:Role of endogenous enkephalins in locomotion and nociception studied with peptidase inhibitors in two inbred strains of mice (C57BL/6J and DBA/2J). 271 68

Recent findings concerning the time-course of opioid-mediated social conflict analgesia have revealed the existence of two distinct nociceptive phases. Analgesia lasting between 30-45 minutes postattack is evident in the early phase whilst hyperalgesia is observed in the late phase at around 70-75 min postattack. This pattern of nociception has similarities with that envisaged in the Perceptual-Defensive-Recuperative (PDR) model of fear and pain and is predictive of defense/fear reactions being seen whilst animals are analgesic with recuperative behaviours becoming evident in the hyperalgesic phase. Detailed ethological analysis was conducted on DBA/2 mice exposed to opioid-activating attack parameters in a resident-intruder paradigm and tested in the presence of a nonaggressive conspecific. During the analgesic phase, at 10 min postagonistic encounter, a profile was observed consisting largely of increased measures of static, self-directed, possibly recuperative, behaviours (immobile crouch and autogrooming). In contrast, during the hyperalgesic phase, at 70 minutes postencounter, there was evidence of increased environmental exploration, attending to and avoiding nonaggressive conspecifics but no increases in autogrooming or any other behaviours that could be viewed as being recuperative. It is concluded that under present test conditions, using DBA/2 mice exposed to opioid activating attack parameters, predictions based on the PDR model of fear and pain are not supported.
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PMID:Hyperalgesia following agonistic encounters in DBA/2 intruder mice is not associated with recuperative behaviours. 275 35

In this study, mechanisms of pain inhibition (tail-flick test) and memory (place avoidance paradigm) were investigated in attacked, DBA/2 and C57BL/6, mice. During training, exposure of test animals to 10 or 30 bites by an aggressive, isolated ICR mouse situated in the dark half of a bright/dark conditioning box induced a significantly higher social conflict analgesia in DBA than in C57 mice. Naltrexone (0.5 and 2.0 mg/kg) reduced this response in DBA mice that received 30, but not 10, bites and was ineffective in C57 mice. This points to different, opioid versus naltrexone-insensitive nonopioid, analgesic mechanisms. During place choice testing in the same box 24 h later, DBA mice that had received 30, but not 10, bites showed a significant, naltrexone-reversible, avoidance of the attack place. No place avoidance learning was observed in C57 mice. The data provided unequivocal evidence that place avoidance learning was a result of associative conditioning, in that neither pairing nor social conflict per se significantly changed the preference for the dark side seen in experimentally naive DBA mice. Antagonism of place avoidance conditioning was observed regardless of whether testing was carried out in the drugged or undrugged state, excluding possible state-dependent effects as an explanation for the naltrexone-induced impairment. Individual correlational analysis in saline-injected, attacked DBA mice revealed a negative relationship between the analgesic state immediately after training and the avoidance of attack place during testing. In summary, the results suggest strain-dependent analgesic and learning mechanisms and indicate that endogenous opioids released in attacked DBA mice support pain inhibition and modulate the memorization of attack place by their analgesic effects, as well as by mechanisms independent of pain inhibitory systems.
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PMID:Place avoidance learning and stress-induced analgesia in the attacked mouse: role of endogenous opioids. 275 88

During development the C57BL/6 and DBA/2 mouse strains present morphological variations in cholinergic forebrain structures correlated with different behavioral reactivities to cholinergic agents. The present research assessed that these strain-dependent differences are also present in cholinergic-mediated analgesia. The administration of oxotremorine (0.0025, 0.005 and 0.01 mg/kg) to 30- and 60-day-old C57 and DBA mice resulted in dose- age- and strain-dependent analgesia. In particular oxotremorine is more effective in DBA/2 than in C57BL/6 mice and the latter strain showed a significant decrease of analgesic response in adulthood.
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PMID:Developmental differences of antinociceptive effects of oxotremorine in two inbred strains of mice. 279 Dec 64

Manipulations of attack parameters in murine agonistic encounters have shown that moderate attack terminating at the first unambiguous display of the upright submissive posture results in nonopioid analgesia. By contrast, attack continuing significantly beyond this behavioural marker results in decreases in nociception mediated by opiodergic mechanisms. However, these effects have only been demonstrated immediately upon termination of encounters. As such, little is known of the influences of agonistic encounters on nociceptive responding beyond this. Tail-flick latencies of male DBA/2 mice that had been exposed to opioid activating attack parameters were established at 15-minute intervals up to 90 min postattack. Data suggest the existence of at least two distinct phases in nociceptive responding with 1) analgesia being evident in the early phase (0-45 min) and 2) short-lasting (detectable only at 75 min postattack) hyperalgesia in the late phase. Further studies revealed both of these effects to be reversed by low (1-10 mg/kg) doses of naloxone. Interestingly, alterations in responsivity to noxious stimulation postmorphine (1-20 mg/kg) administration followed a similar pattern, with analgesia being detectable 0-2 hr and hyperalgesia being evident at 4 hr postinjection of either 10 or 20 mg/kg morphine. However, only the hyperalgesia induced by 20 mg/kg morphine was reversed by 10 but not 1 mg/kg naloxone. These data together suggest a relationship between the dose of morphine required to induce hyperalgesia and the amount of naloxone needed to reverse this response. The naloxone-reversibility of postencounter or morphine-induced hyperalgesia suggests that these effects are not a consequence of the absence of opiates/opioids per se.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Naloxone-sensitive hyperalgesia follows analgesia induced by morphine and environmental stimulation. 279 44

The pattern of sensitivity of mice from three inbred strains were compared on measures of morphine-induced analgesia (hot plate), locomotor activity, hypothermia, Straub tail (muscular rigidity), antidiuresis and constipation. The DBA/2J strain emerged as the most sensitive strain for analgesia, retention of a water load (antidiuresis) and hypothermia. In addition, the DBA/2J mice had lower concentrations of morphine in the brain 30 min after injection and had the lowest Kd and the highest Bmax for naloxone as measured by in vitro receptor binding. In contrast, mice of the C57BL/6J strain were most sensitive when locomotor activity, Straub tail and constipation were measured. The C3H/HeJ mice were generally intermediate in their sensitivity to morphine. The observed strain differences indicate a rather high degree of genetic control for most of the effects studied, however, the low consistency of rank order among the three strains across these measures suggests that the genetically determined mechanisms are largely different between these measures of morphine sensitivity.
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PMID:Genetic dissociation of multiple morphine effects among C57BL/6J, DBA/2J and C3H/HeJ inbred mouse strains. 281 56


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