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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the locomotor-enhancing action of mu-opioid receptor agonists, such as morphine and [D-Ala2, N-MePhe4, Gly-ol5]enkephalin (DAMGO), and physical dependence on morphine in diabetic and nondiabetic mice. Morphine (5-20 mg/kg, s.c.) and DAMGO (1-4 nmol, i.c.v.) had a dose-dependent locomotor-enhancing effect in both nondiabetic and diabetic mice. The locomotor-enhancing effects of morphine and DAMGO were significantly less in diabetic mice than in nondiabetic mice, and were significantly reduced after pretreatment with either beta-funaltrexamine (20 mg/kg, s.c.), a selective mu-opioid receptor antagonist, or naloxonazine (35 mg/kg, s.c.), a selective mu1-opioid receptor antagonist. Both diabetic and nondiabetic mice were chronically treated with morphine (8-45 mg/kg, s.c.) for 5 days. During this treatment, neither diabetic nor nondiabetic mice showed any signs of toxicity. After morphine treatment, withdrawal was precipitated by injection of naloxone (0.3-10 mg/kg, s.c.). Several withdrawal signs, such as weight loss, diarrhea, ptosis, jumping and body shakes, were observed after naloxone challenge in morphine-dependent nondiabetic mice. Although morphine-dependent diabetic mice showed greater weight loss than nondiabetic mice, the incidence of jumping and body shakes after naloxone challenge in diabetic mice were lower than that in nondiabetic mice. These results suggest that diabetic mice are selectively hyporesponsive to mu1-opioid receptor-mediated locomotor enhancement. Furthermore, diabetes may affect mu1-opioid receptor-mediated naloxone-precipitated signs of withdrawal from physical dependence on morphine.
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PMID:Modification of mu-opioid agonist-induced locomotor activity and development of morphine dependence by diabetes. 763 31

The effect of perinatal lead exposure (at 300 and 1000 ppm in the maternal drinking water from conception to postnatal day 14) on the opioid withdrawal syndrome in adult offspring has been studied to assess if lead produces long term disruption of opioid systems manifested as altered morphine dependence. Dependence was induced in 50 day old rats by administration of morphine in osmotic mini-pumps implanted subcutaneously and delivering 5, 15 or 40 mg/kg/day. At postnatal day 55 an opioid withdrawal syndrome was precipitated by administration of naloxone (4 mg/kg i.p) and withdrawal behaviour scored over the next 30 min. Both objective (jumping, weight loss, weight of excreta, wet dog shakes, mouthing and face washing) and subjective (teeth chatter, ptosis, diarrhoea, irritability) measures were scored. 60 min after naloxone animals were killed and plasma corticosterone measured as a biochemical index of withdrawal. Morphine withdrawal scores and plasma corticosterone exhibited a clear dose relationship and there were no significant differences between 0 and 300 ppm lead-exposed groups. However withdrawal scores in 1000 ppm lead-exposed animals were lower in 15 and 40 mg/kg morphine treated rats, predominantly associated with lower weight loss, wet dog shakes and mouthing responses. Paradoxically corticosterone levels were elevated in the 40 mg/kg morphine dose group. The results support other evidence that perinatal lead exposure can induce disruption in opioid functioning which persists to adulthood and suggest a possible link between lead and opioid addiction.
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PMID:Effect of perinatal lead treatment on morphine dependence in the adult rat. 824 87

Clinical studies have suggested that patients who take morphine for pain relief do not show a high degree of dependence. The present study examined the development of naloxone-precipitated withdrawal in rats receiving morphine in the presence or absence of formalin-induced pain. Morphine (10 mg/kg, i.p.) or saline was administered for 4 consecutive days 10 min after a subcutaneous injection of 50 microliters of 2.5% formalin or saline into the hind-paw. On the 5th day, rats were injected with naloxone (1 mg/kg, i.p.) and observed for signs of precipitated withdrawal (ptosis, teeth chattering and excretion/diarrhea). Naloxone-precipitated withdrawal symptoms were significantly greater in rats that received morphine in the absence of pain than in rats that received morphine in the presence of pain.
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PMID:Formalin-induced pain antagonizes the development of opiate dependence in the rat. 827 66

Postnatal day-14 (P14) infant rats remained naive or were implanted with osmotic minipumps infusing saline or fentanyl (50 microg kg(-1) h(-1)). Fentanyl was administered 72 h later for measurement of antinociception in the tail-flick test. The potency of fentanyl was 3.0-fold lower in fentanyl-infused compared to saline-infused P17 rats. Fentanyl-infused P17 rats injected with naloxone underwent withdrawal characterized by increases in spontaneous activity, wall climbing, diarrhea, abdominal stretching, forepaw treading/tremors, wet-dog shakes, jumping, ptosis, rhinorrhea and hypothermia. Other naive, saline-infused and fentanyl-infused P17 rats not challenged with fentanyl or naloxone were housed until maturing into P42 juveniles. Fentanyl's potency was equal among each treatment group. However, morphine's potency was reduced in juveniles tolerant to fentanyl as infants. Morphine was also less potent in P90 adults tolerant to fentanyl as infants. Thus, chronic opiate exposure during infancy may affect the developing central nervous system, and desensitize animals and humans to opiate analgesia throughout life.
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PMID:Long-term alterations in opiate antinociception resulting from infant fentanyl tolerance and dependence. 988 76

The present study examined the effect of the gamma-aminobutyric acidB (GABA(B)) receptor agonist, baclofen on naloxone-induced withdrawal signs in morphine-dependent rats and modification by the antagonist, 3-aminopropyl-cyclohexylmethylphosphinic acid (CGP 46381). Morphine was administered via mini-osmotic pumps for 7 days to induce physical dependence. Baclofen (20 mg kg(-1)) decreased stereotyped head movements, chewing, chatter, ptosis and body weight loss, induced by naloxone (10 mg kg(-1)) in morphine-dependent rats. CGP 46381 (20 mg kg(-1)) reversed the effects exerted by baclofen on stereotyped head movements, ptosis, and weight loss and partially reversed the effect of baclofen on chewing. It can be concluded that baclofen has some potential in the treatment of opioid withdrawal and that GABA(B) receptors may be implicated in such a withdrawal.
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PMID:Attenuation of morphine withdrawal signs by the GABA(B) receptor agonist baclofen. 1179 9

This work was performed to clarify the differences between a long or short development of morphine dependence as well as between a recently installed or a long-term dependence. Morphine withdrawal in rats is a well-characterized phenomenon but this is not so in mice. A study of the principal withdrawal signs have been performed in mice, evaluating their specificity and particular profile of appearance in each type of dependence. Mice were divided into two groups that received increasing doses of morphine every 24 h, three groups that received increasing doses of morphine twice a day for 3 days, and a control group that received saline. Naloxone-induced opiate withdrawal was evaluated following short-term exposition to morphine [Test 1 (T1)--saline and Test 2 (T2)--naloxone] and long-term exposition to morphine [Test 3 (T3)--naloxone and Test 4 (T4)--saline]. Morphine administration twice a day is more effective in inducing opiate dependence than once a day, and with the latter, the duration of morphine exposure increases the intensity of withdrawal signs. Weight loss, diarrhea, body shakes, jumping, paw tremor, ptosis, piloerection, and the modified Gellert-Holtzman scale for mice are specific patterns of naloxone-induced withdrawal. The first four signs allow the discrimination between different levels of opiate dependence. Body care, piloerection, and the modified Gellert-Holtzman scale could be useful to detect conditioned withdrawal.
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PMID:Ethological analysis of morphine withdrawal with different dependence programs in male mice. 1181 12

Glutamate has a key role in pain perception and also development of tolerance and dependence to morphine. It has been reported that clavulanic acid affects glutamatergic transmission via activation of glutamate transporter. Therefore the present study was aimed to evaluate the possible antinociceptive effect of clavulanic acid and its preventive activity against development of morphine tolerance and dependence in animal models. Male Swiss mice (25-30 g) were used in this study. Acetic acid-induced writhing, formalin test and hot plate method were used to assess the antinociceptive effect of clavulanic acid. Morphine (30 mg/kg, s.c.) was administered to the mice two times a day (8 AM and 4 PM) for 3 days in order to produce tolerance. To develop morphine dependence, morphine sulfate (50, 50 and 75 mg/kg) was injected at 8 and 12 AM and 16 PM respectively and for 3 consecutive days. Naloxone (5 mg/kg, i.p) was used to induce morphine withdrawal syndrome and the number of jumps and presence of ptosis, piloerection, tremor, sniffing and diarrhea were recorded and compared with control group. Clavulanic acid at doses of 10, 20 and 40 mg/kg inhibited abdominal constriction and licking behavior of acetic acid and formalin-induced pain respectively. Clavulanic acid was not able to show any antinociception in hot plate model and could not prevent development of tolerance and dependence to morphine. Clavulanic acid has considerable antinociceptive activity and further studies are needed to clarify its exact mechanism.
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PMID:Antinociceptive effect of clavulanic acid and its preventive activity against development of morphine tolerance and dependence in animal models. 2565 3