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Query: UNIPROT:Q86TM3 (cage)
29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Characteristics of changes in ambulatory activity after repeated administration of morphine, 5, 10 or 20 mg/kg s.c., were investigated in male mice of dd strain. The drug was administered 10 times at intervals of 1, 3-4 or 7 days, and the ambulatory activity of each mouse was measured by a tilting-type round activity cage with a 25 cm diameter for 180 min after each administration. Morphine, 5-20 mg/kg induced a dose-dependent increase in the ambulatory activity, and this effect attained to a peak at 60-90 min and persisted for 120-180 min after the administration. An augmentation of sensitivity (a reverse tolerance) to the ambulation-increasing effect of morphine was induced by the repeated administration of 10 and 20 mg/kg morphine, regardless of the intervals. The reverse tolerance achieved the maximum on the 5-6th administration day, and almost the same level of sensitivity was maintained until the 10th administration day. There was no significant difference in the activity counts at the peak time among the groups of mice varying the administration intervals. However, the persistence of increased ambulatory activity tended to be longer in the group of mice given morphine at intervals of 7 days than in the group given it at intervals of 1 day. The reverse tolerance, once produced, attenuated 2 months after the cessation of the repeated administration. However, the ambulatory activity counts did not return to those on the 1st administration day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Development and characteristics of reverse tolerance to repeatedly administered morphine in mice manifested by enhanced motor activities]. 666 19

Effects of repeated administration of morphine on ambulatory activity were studied in mice treated with morphine-admixed food. The ambulatory activity was determined by the tilting cage method. Morphine injection (10 mg/kg s.c.) was repeated at 3-4 day intervals. The ambulatory activity was enhanced progressively when morphine was repeatedly given to mice. However, the enhancing effect was not observed in mice treated with morphine-admixed food (1 mg/g food). These results suggested that the reverse tolerance to morphine did not develop under the condition of exposure to morphine by DAF (drug-admixed food) method. In case of treatment with morphine-admixed food of increasing concentration (1,2 and 3 mg/g food), the ambulatory activity of morphine was decreased. According to the studies done so far, tolerance development to the stimulant effects was not observed. This study demonstrates that the tolerance develops to the stimulant effects of morphine on the schedule of treatment with morphine of increasing doses by the DAF method.
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PMID:[Motility effects of morphine in morphine-tolerant mice by the DAF method]. 668 17

Separation-induced calling in the young of many species can be modulated by the opioid system. Morphine reduces ultrasonic vocalizations (USVs) produced by isolated rat pups, an effect blocked by naltrexone. Central administration of the mu and delta opiate receptor agonists DAMGO and DPDPE reduce USV; kappa receptor agonist U50,488 increases them. We now find that peripheral U50,488 not only boosted calling rates in isolated 3-, 10-, and 18-day-old rat pups, but also induced calling in pups of these ages tested in the home cage with their littermates, where USVs are seldom heard in nature. U50,488 lowered rectal temperature, although temperature loss and USV were not correlated within drug treatment groups.
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PMID:U50,488 increases ultrasonic vocalizations in 3-, 10-, and 18-day-old rat pups in isolation and the home cage. 811 89

Ultrasonic vocalizations may be an expression of the affective pain response in laboratory animals. The present experiment compares the effects of morphine to the delta agonist, DPDPE (D-Pen2,D-Pen5 enkephalin) on a range of reflexive, behavioral and affective responses during an aggressive interaction. In experiment 1, naive female Long-Evans rats received morphine (0, 1, 3, 6, 10 micrograms ICV), or DPDPE (0, 30, 60, 100 micrograms ICV). In experiment 2, female rats were treated with naltrindole (1.0 mg/kg IP) 20 min before DPDPE (0, 60, 100 micrograms ICV). The following endpoints were measured: (1) latency to tail flick in response to heat stimuli; (2) high (33-65 kHz) and low (20-32 kHz) frequency ultrasonic and audible vocalizations; (3) defensive behavior; and (4) motoric activity. Following a brief exposure to attack, rats were threatened by the aggressor but protected from further attack by a large, wire mesh cage, thereby allowing for continued behavioral and vocal measurement without the risk of physical injury; video and audio recordings were made during the attack and then during a portion of the protected encounter (2 min). Morphine suppressed pain reactions varying in complexity from a spinal reflex, to an organized escape reaction, to an affective vocal response. The delta agonist, DPDPE, attenuated high frequency ultrasonic calling and tail flick responding. Defensive behaviors were also modulated by DPDPE at doses that had no effect on walking or rearing, indicating behavioral specificity. By contrast, doses of morphine that decreased defensive upright and escape also decreased motor activity. In female rats, morphine and DPDPE share a common profile of effects on a range of functional end-points, but DPDPE appears to modulate more selectively the reactions related to aversiveness without exerting sedative effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Delta opioid receptors: reflexive, defensive and vocal affective responses in female rats. 854 26

When morphine administration is paired with a distinctive context, tolerance to morphine's analgesic effects comes readily under the associative control of the drug-paired context. These associative tolerance effects are eliminated when a relatively short (i.e., 6 h) interdose interval (IDI) is used for conditioning. Contemporary models of learned tolerance explain the absence of learning at short IDIs by positing that residual morphine effects from a recent drug exposure disrupt the formation of drug-context associations. The present studies examined the impact of unsignaled morphine injections given 6 h prior to drug-context pairings on the development of associative tolerance. Analgesia was measured by the tail-flick method, and tolerance levels were assessed by dose-response curve methodology. Morphine preexposure had no detectable influence on the acquisition of associative tolerance when rats were tested immediately after conditioning, after a 30-day rest interval, or after a 30-day period of daily saline injections in their home-cage environment. These data suggest disruption of associative tolerance effects at short IDIs is not attributable to residual effects of morphine from the immediately preceding trial.
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PMID:Unsignaled morphine delivery does not disrupt the development of associative morphine tolerance in the rat. 874 31

Morphine significantly impairs maternal behavior; naloxone, an opiate antagonist, restores it. Maternal behavior is associated with c-fos expression, an immediate early gene product, in the medial preoptic area (mPOA) of females. In two experiments, the effects of morphine-alone and morphine plus naloxone on the expression of c-fos were examined. On postpartum day 5, females were injected with morphine or saline (experiment 1), and morphine + naloxone or morphine + saline (experiment 2) and placed back in the home-cage, separated from their pups by a wire-mesh partition. A separate group in experiment 1 was injected but not exposed to pups. Processing for c-fos immunohistochemistry commenced, and c-fos positive cells in a proscribed portion of mPOA were counted. Morphine-treated females had fewer c-fos cells in mPOA compared to saline-treated females, and the presence of pups accounted for a significant increase in c-fos-expressing neurons, whereas in females not exposed to pups, morphine treatment did not significantly reduce baseline c-fos expression (experiment 1). Furthermore, naloxone mitigated the effect as morphine + naloxone-treated females expressed more c-fos cells compared to morphine + saline females (experiment 2). Morphine-treated females, therefore, may exhibit reductions in maternal behavior because of relative opiate-induced inactivation of areas of the brain devoted to the regulation of maternal behavior.
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PMID:Opiate disruption of maternal behavior: morphine reduces, and naloxone restores, c-fos activity in the medial preoptic area of lactating rats. 951 Apr 24

Morphine action in the periaqueductal gray (PAG) matter of the mesencephalon suppresses T cell proliferation and NK cell activity through actions at mu opioid receptors. We investigated the effect of acute microinjection of morphine in the rat PAG on macrophage function. We found that morphine injection in the PAG significantly (p <.01) suppressed nitric oxide production by untreated (82 +/- 23% suppression), IFN-gamma-primed (57 +/- 11% suppression), and LPS-activated (50 +/- 7% suppression) splenic macrophages and did not alter macrophage viability. In contrast, IFN-gamma- and LPS-activated macrophages from PAG-injected saline rats generated an increased output of nitric oxide, which was associated with significant (p <.01) reduction in cell viability. Morphine significantly (p <.01) inhibited TNF-alpha production by LPS-activated macrophages (28 +/- 8% inhibition compared with PAG-injected saline rats). In addition, morphine significantly (p <. 05) inhibited phagocytosis of Candida albicans by resident macrophages (40 +/- 20% inhibition compared with that of macrophages from PAG-injected saline rats). Responses of resident or activated macrophages from PAG-injected saline and untreated control groups did not differ significantly. The results of this ex vivo study suggest that suppressive effects of morphine on macrophage functions may contribute to increased susceptibility to infectious diseases and cancer associated with drug abuse.
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PMID:Suppression of splenic macrophage functions following acute morphine action in the rat mesencephalon periaqueductal gray. 1046 23

The long-term effects of postnatal manipulation on nociception were studied in NMRI albino male mice. During the first two weeks of life, pups were removed from their cage and deprived of maternal/nest odour for 15 min/day. To evaluate pain sensitivity, adult mice exposed to this postnatal manipulation (CB group) were tail flick and formalin tested for acute and tonic pain, respectively. CB mice showed a reduced pain sensitivity both in tail-flick and in formalin tests in comparison with control animals. Moreover, responsiveness to morphine (MO 1.0, 2.5, and 5.0 mg/kg, i.p.) in young (35 days old) and adult (90 days old) postnatally manipulated animals was evaluated with the tail-flick test: a decrease of the antinociceptive effects induced by morphine both in young and adult males was observed in postnatally manipulated animals. Morphine induced significant analgesic effects in control mice at doses lower than those affecting nociceptive thresholds both in young and adult CB mice. In addition, young animals showed a higher sensitivity to morphine than adults, independently of postnatal manipulation. The long-term effects of postnatal manipulation on nociception are discussed in terms of involvement of the opioid system and of the characteristics of pup manipulation.
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PMID:Effects of postnatal manipulation on nociception and morphine sensitivity in adult mice. 1053 27

This study examined the possibility that cadmium, a toxicant in high concentration in all tobacco products, may alter the stimulus properties of morphine. Adult male rats were exposed to regular laboratory chow (Group Control) or chow containing 100 ppm added cadmium chloride (Group Cadmium). Following an initial 30 day exposure period, control and cadmium-exposed animals were trained to discriminate between i.p. injections of 3.00 mg/kg morphine sulfate and vehicle (distilled water) in a two-choice drug discrimination task. Subsequently, the morphine dose-effect generalization function (0.75-6.00 mg/kg) was determined for control and cadmium-exposed animals. Additional substitution tests were conducted with increasing doses of the high efficacy mu agonist fentanyl (0.0016-0.04 mg/kg), the intermediate efficacy mu agonist (-)-metazocine (0.60-5.00 mg/kg), and the kappa agonist (+/-)-bremazocine (0.03-0.12 mg/kg). Also, increasing doses of the selective mu antagonist naloxone (0.0008-0.50 mg/kg) were presented against the training dose of morphine (3.00 mg/kg) and 0.02 mg/kg fentanyl. Finally, training was discontinued, and control and cadmium-exposed animals were injected with 8.00 mg/kg morphine in the home cage every 12 hr for 2 weeks, prior to redetermining the morphine dose effect function. Following a 1 week recovery period where morphine injections were discontinued, a final determination of the morphine dose-effect function was made. The results of the investigation indicated that cadmium exposure, without affecting the rate-changing properties of the drugs, slowed initial acquisition of the morphine discrimination, decreased the potency of selective doses of naloxone with respect to antagonizing the stimulus effects of morphine and fentanyl, and blocked the development of tolerance to morphine. Morphine, fentanyl, and (-)-metazocine generalized (substituted) equally across both groups, while (+/-)-bremazocine failed to substitute for the morphine stimulus in either group. These findings add to the growing literature on the interaction between metal poisoning and drug selection/abuse.
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PMID:Dietary cadmium exposure alters characteristics of training, substitution, and tolerance when morphine is used as a discriminative stimulus. 1102 63

Given that social influences are among the strongest predictors of adolescents' drug use, this study examines the effects of social interactions on morphine sensitization in both adolescent and adult rats. Rats treated with morphine (twice daily, 6 days, 2.5-10 mg/kg, subcutaneously, s.c.) or saline were group-housed in two different conditions. Thus, four experimental groups were examined for each age group: (1) morphine-treated rats housed physically and visually separate from saline-injected rats ('morphine only'); (2) morphine-treated rats housed together with saline-injected rats ('morphine cage-mates'); (3) saline-injected rats housed together with morphine-treated rats ('saline cage-mates'); and (4) saline-injected rats housed physically and visually separate from morphine-treated rats ('saline only'). Starting 9 days following the last morphine injection, rats were individually examined once daily for 5 consecutive days for their locomotor response to 2.5 mg/kg of morphine. For both age groups, there were no significant differences in morphine-induced hyper-locomotion between saline cage-mates and saline only rats. Morphine only rats exhibited morphine locomotor sensitization as compared to both the saline only and saline cage-mates rats. Notably, a significant difference was observed between the adolescent morphine cage-mates and morphine only rats. The adolescent morphine cage-mates did not exhibit the enhanced locomotor response as compared to the saline only and saline cage-mate rats. A trend of reduced morphine locomotor sensitization was observed in the adult morphine cage-mates as compared to morphine only but it did not reach statistical significance. Thus, this study demonstrates social influences on morphine sensitization which are more prevalent in adolescents as compared to adults.
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PMID:Social influences on morphine sensitization in adolescent rats. 2150 52


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