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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence suggests a close relationship between ACTH and opioids. They are derived from the same precursor molecule, released concomitantly in response to stress and are known to interact at receptor level. Acute exposure to endogenous opioids induces analgesia in the short-term yet shifts the morphine dose-response curve to the right for a period of several weeks. Therefore, the possibility exists that ACTH might also exert an influence extending beyond that suggested by its biological half-life. To investigate this further, DBA/2 mice were pretreated with porcine ACTH left undisturbed for 3 days, then challenged with morphine. Dose-response studies indicated that pretreatment with 10 but not 0, 0.1 or 1.0 IU ACTH influenced responsivity to morphine, rendering a sub-analgesic dose (1.0 mg/kg) effective and significantly enhancing the degree of analgesia observed following treatment with 5 mg/kg morphine, suggesting a shift in the dose-response curve to the left. Time-course analysis revealed 5 mg/kg morphine to induce an analgesic reaction with an onset of between 15-30 and lasting between 60 and 120 min post opiate administration. ACTH pretreatment did not influence this time course, however a significantly greater degree of analgesia was observed at 60 min post morphine injection in 10 IU ACTH pretreated animals than in saline pretreated controls. ACTH pretreatment further influenced subsequent responding to chronic morphine administration. Whilst saline pretreated animals demonstrated significant analgesia in response to the first administration, tolerance to this effect had developed following four days of repeated exposure to morphine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ACTH: a single pretreatment enhances the analgesic efficacy of and prevents the development of tolerance to morphine. 283 53

Mice of the inbred strain DBA/2, when exposed to a social conflict, developed a low intensity, naloxone-insensitive analgesia after 15 bites, and a more pronounced naloxone-sensitive analgesia after 45 bites. The effective inhibition of the antinociceptive response following low and high number of bites by the alkylating opiate antagonist beta-chlornaltrexamine suggests participation of opioid mechanisms at both stress levels. Emergence of an increased tail-flick latency was indicated by the occurrence of defensive upright postures upon contact with the opponent, while animals displaying full analgesic response during the period of bite 31-45 increased their escape reactions without being in contact with the aggressor. Suppression of social conflict analgesia in mice by pretreatment with opiate antagonists facilitated the occurrence of these escape reactions. The display of panic escape responses is discussed in the context of increased fear and helplessness that developed under conditions of sustained attacks.
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PMID:Emergence and development of stress-induced analgesia and concomitant behavioral changes in mice exposed to social conflict. 285 47

The effects of hashish extract on adaptive behavior of male mice were studied in a paradigm which allows the investigation of learning mechanisms in a social context. Mice of the C3H strain, which were not submissive in a confrontation with a nonaggressive DBA mouse on day 1, were defeated on day 2 over 3 min by aggressive, isolated DBA mice, and showed conditioned submissive behavior upon mere contact with a nonaggressive DBA mouse on day 3. A hashish extract containing 38.6-39.4% delta 9-tetrahydrocannabinol (delta 9-THC), 11.6-12.0% cannabinol and 47.7-48.5% cannabidiol was administered orally in all experiments. Hashish extract given 90 min before defeat on day 2, in dosages corresponding to 1, 5, and 10 mg delta 9-THC/kg, impaired retention of defensive upright, defensive sideways and immobility on day 3 (experiment 1). Experiment 2 showed that the drug (5, and 10 mg delta 9-THC/kg) had no antinociceptive potency in mice and did not modify defeat-induced analgesia. Experiment 3, with drug (5 mg delta 9-THC/kg) or solvent administration on day 2 and day 3, showed that the retention deficit was neither due to state-dependent learning, nor to impaired retrieval. It is suggested that hashish extract administered before learning may interfere with memory processing.
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PMID:Hashish extract impairs retention of defeat-induced submissive behavior in mice. 299 43

In a first experiment, exposure of DBA/2 mice to a small number of attack bites by a C57BL/6 mouse resulted in low-intensity analgesia as assessed by the tail-flick test. The analgesia dissipated within 10 min and was insensitive to naloxone (10 mg/kg, sc) but was antagonized by the irreversible opioid antagonist beta-chlornaltrexamine (5 mg/kg, sc). In a second experiment, preexposure to a nonaggressive C57BL/6 opponent prevented low-intensity analgesia induced by a small number of attack bites 24 hr later. The preexposure effect was abolished by naloxone (10 mg/kg, sc) given before the nonaggressive confrontation. This suggests that the release of endogenous opioids during preexposure interferes with the subsequent activation of endogenous opioid-mediated pain control mechanisms.
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PMID:Preexposure to a nonaggressive opponent prevents low-intensity, social-conflict analgesia in mice. 303 38

The present study characterizes the time course of social conflict analgesia and its reversibility by opioid antagonist drugs in the C57BL/6 and DBA/2 inbred strains of mice and examines the relationship between alterations in brain and pituitary levels of beta-endorphin-like immunoreactivity (beta-ELIR) and the antinociception elicited by social stress. Data revealed statistically significant strain differences in regard to beta-ELIR in control animals. The pituitary content of beta-ELIR was higher in DBA/2, while the values in the periaqueductal grey (PAG) and in the amygdala were higher in C57BL/6 mice. No interstrain differences were found in the hypothalamus. Exposure to 50 attack bites resulted in a 6-fold higher analgesia in DBA/2 mice and in a strain-independent fall of beta-ELIR in pituitary (approximately 27%) and PAG (23%). PAG but not pituitary beta-ELIR levels in C57BL/6 mice correlated positively with the increase in tail-flick latency after attack. Mere confrontation with a non-aggressive opponent failed to induce analgesia and was associated in C57BL/6 mice with a significant reduction in the beta-ELIR content of both the pituitary and the PAG. The data are discussed in terms of genotype-dependent sensitivity of the beta-endorphin system to stress and its relation to analgesia.
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PMID:Social conflict-induced changes in nociception and beta-endorphin-like immunoreactivity in pituitary and discrete brain areas of C57BL/6 and DBA/2 mice. 340 13

Four experiments were designed to characterize long-term analgesic (LTA) reaction in attacked mice. In Experiment 1 we showed that analgesic reaction in DBA mice, induced by the stress of being attacked (30 or 50 bites), is reinstated upon reexposure to seven bites 24 hr later. The magnitude of the LTA response depended on the level of analgesia on Day 1 and was smaller than the original response. In Experiment 2 we showed that LTA was prevented by naloxone or beta-chlornaltrexamine given before exposure (50 bites) on Day 1. Results of Experiment 3 revealed that naloxone or beta-chlornaltrexamine injected before reexposure to seven bites on Day 2 antagonized LTA measured 10 min, but not 1 min, after reexposure. In Experiment 4 we showed that morphine substituted for being attacked on Day 1 failed to produce LTA. We concluded that pain inhibitory mechanisms remain in a state of increased readiness for at least 24 hr after attack stress and that activation of opioid systems is necessary but not sufficient to produce LTA, a response that is only partly sensitive to opioid antagonists.
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PMID:Long-term analgesic reaction in attacked mice. 342 95

Behavioral reactions (submissive postures, escape, immobility, activity, locomotion) in C57BL/6 and DBA/2 test mice were recorded during single (50 bites) or three repeated (3 X 50 bites, separated by 24 hr) aggressive confrontations, as well as during a nonaggressive confrontation 24 hr after the last aggressive confrontation with opponents of the opposite strain. Nociception (hot plate response latency) was measured 1 min after aggressive or nonaggressive confrontations. During repeated aggressive confrontation, DBA mice reacted with a stable pattern of escape and analgesia, whereas C57 mice failed to develop an analgesic response and changed their behavioral defense strategy during repeated aggressive confrontations (decrease of escape, increase of defensive upright). The conditioned display of submission and of escape behavior during nonaggressive confrontation did not change as a function of earlier repeated aggressive confrontations in DBA mice, while C57 mice showed a significant increase of defensive upright postures and immobility. Conditioned analgesia was not observed after nonaggressive confrontations. The results point toward a dissociation between attack-elicited behavior and antinociception and suggest that encounter-induced analgesia may influence the processing of aversive experience.
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PMID:Effects of repeated as compared to single aggressive confrontation on nociception and defense behavior in C57BL/6 and DBA/2 mice. 358 5

Exposure to repeated attack induces a long-lasting analgesia in male mice. Although this reaction has been linked to the special biological significance of defeat, earlier research has confounded defeat and exposure to further attack. In the present studies, DBA/2 intruder mice were individually placed into the home cages of aggressive conspecifics and removed immediately upon display of the species-characteristic upright submissive posture. Under these test conditions, intruders did indeed show a profound analgesia. However, in marked contrast to the antinociceptive effects of repeated attack, this reaction was of short duration (less than 10 min), was not blocked by naloxone (1-10 mg/kg, IP) and did not show cross-tolerance either to or from morphine (5 mg/kg, IP). These findings are discussed in relation to multiple endogenous pain inhibitory systems and their possible adaptive significance in murine social behaviour.
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PMID:Acute non-opioid analgesia in defeated male mice. 371 72

Several doses of tifluadom, an opioid benzodiazepine with affinity for opioid kappa receptors, were tested on analgesia and locomotor activity in two strains of mice, the C57BL/6 and the DBA/2. The analgesic properties of the compound were confirmed in both strains by a tail flick test. As concerns locomotor activity both strains, that in previous researches showed opposite responses to opiates, were depressed by tifluadom, suggesting the involvement of kappa receptors in this effect.
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PMID:Locomotor depression by the opioid benzodiazepine tifluadom in mice. 609 79

Defeat-induced unconditioned and conditioned behaviors of C57BL/6 and DBA/2 mice were assessed in a social-learning paradigm. Upon bites, mice of the DBA strain reacted with significantly more escape reactions, while C57 mice showed more immobility, crouch, and defensive sideways and upright postures. Clear genotype-dependent patterns were also evident from the conditioned responses recorded 24 h after defeat. DBA mice displayed more escape and defensive sideways and upright postures upon contact with a nonaggressive partner mouse; in contrast, C57 mice reacted with more immobility and crouch. With an increasing number of bites the sum of learned responses increased in C57 mice while it decreased in mice of the DBA strain. This decrement was paralleled by an increase in the analgesic response measured on the hot plate in defeated DBA mice. The possible role of endogenous opioids in the genotype-dependent interaction of defeat-induced learned submissiveness and analgesia is discussed.
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PMID:Defeat, learned submissiveness, and analgesia in mice: effect of genotype. 654 55


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