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Although the morphine withdrawal syndrome has been well described in the rat, a syndrome having similar characteristics has not been demonstrated following chronic methadone treatment. In this study we describe the behavioral effects produced by naloxone (4 mg/kg sc) following 72 hours of continuous iv infusion of methadone, (12.2 micrograms/kg/min), morphine (12.2 to 97.9 micrograms/kg/min) or saline. The cessation of methadone or morphine but not saline treatment followed by naloxone resulted in graded signs including wet dog shakes, escape attempts, self-stimulation and body weight loss and quantal signs including diarrhea, ear blanching, exophthalmos, ptosis, tachypnea and teeth chattering. These results indicate that this mode of methadone administration produces physical dependence characterized by a morphine-like withdrawal syndrome in the rat.
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PMID:Methadone induced physical dependence in the rat. 653 54

The drug-admixed food method was applied to ICR strain mice for studying development of physical dependence on morphine. Mice were treated with morphine-admixed food of increasing concentration (1, 2 and 3 mg/g food) every third day for 9 days. During the treatment, the mice did not show any signs of toxicity. Plasma and brain morphine levels were quantitatively related to the morphine concentration in drug-admixed food. The plasma morphine level showed a circadian rhythm, and the level was higher than 0.15 microgram/ml throughout the day. The morphine-treated mice manifested body weight loss, diarrhea and ptosis from 4 hr after morphine withdrawal and showed maximum body weight loss at 12 hr. In the naloxone-precipitated test, jumping and body shakes were observed in mice treated with morphine-admixed food (2 mg/g food) at least for 1 day. Moreover, in mice treated with morphine (2 mg/g food) for 3 days, marked jumping and body shakes and some writhing were observed after naloxone administration. These results suggest that the drug-admixed food method has advantages of easily and rapidly inducing the physical dependence on morphine in mice without causing toxicity and death.
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PMID:Induction of physical dependence on morphine in mice by the drug-admixed food method. 653

The developmental process of physical dependence on codeine has been explored in rats treated with codeine-admixed food (0.5 mg/g food) during 1 to 7 days. In rats treated with codeine for more than 2 days, body weight loss was markedly observed after the abrupt codeine withdrawal. The intensity and time course of body weight loss increased according to the duration of codeine treatment. After the codeine withdrawal, behavioral signs such as diarrhea, ptosis and vocalization were observed. In the naloxone-precipitated withdrawal test, rats treated with codeine for 1 day manifested a loss of body weight after naloxone challenge, and the intensity of body weight loss increased according to the duration of codeine treatment. After naloxone injection, the codeine-treated rats showed abnormal behaviors such as diarrhea, ptosis, teeth chattering , salivation, body shakes, vocalization, nose bleed, irritability, lacrimation and writhing. The total score, evaluated by the ranking system for precipitated withdrawal behaviors, was correlated with the duration of codeine treatment. These results suggest that naloxone-precipitated withdrawal signs are powerful in comparison with that after codeine withdrawal, and the weight loss is a common index for quantitative assessment of physical dependence on narcotics in the natural and naloxone-precipitated withdrawal tests. It is concluded that the drug-admixed food ingestion method has the advantage of rapidly inducing a high degree of physical dependence on codeine.
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PMID:Induction of physical dependence on codeine in the rat by drug-admixed food ingestion. 653 1

A comparison of several methods for developing physical dependence to morphine was made. Male Sprague-Dawley rats were treated with morphine-admixed food (drug-admixed food, DAF; 0.5 and 1 mg/g food), morphine slow release emulsion (SRE; 75, 100 and 150 mg/kg) and morphine (75 mg) pellets. In the SRE and pellet methods, the typical signs of morphine toxicity, such as catatonia, exophthalmos and shallow respiratory movements, were observed 15-20 min after the treatment and these signs were maintained for 14-18 hr. In rats treated with SRE and pellets, plasma morphine levels reached a maximum 1 day after the morphine treatment, and subsequently decreased, while plasma morphine levels in rats treated with DAF increased treatment period-dependently. Withdrawal signs precipitated by naloxone (3 mg/kg, sc) in rats treated with DAF, SRE and pellets were characterized by loss of body weight, shaking, vocalization, diarrhea, ptosis, tooth-chattering, nose bleed, salivation and lacrimation. Naloxone-precipitated withdrawal signs reached a maximum 1-2 days after treatment with SRE and pellets, and were correlated with the duration of DAF treatment. Rats treated with DAF, SRE (150 and 225 mg/kg) and pellets for 3 days, manifested loss of body weight, diarrhea etc. after the morphine withdrawal. Maximum body weight loss in each group was 7-10% at 1-2 days after the morphine withdrawal. It was thus, concluded that physical dependence on morphine can be induced rapidly by these three methods. However, the SRE and pellet methods induced morphine toxicity and it was difficult to maintain physical dependence on morphine in these rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of three methods of inducing physical dependence to morphine in rats using short-term medication]. 654 77

1. The development process of physical dependence on and tolerance to morphine has been explored in rats treated with morphine-admixed food (0.5 mg/g of food) during 1 to 7 days. 2. In the morphine-treated animals, body weight loss was observed after the abrupt morphine withdrawal. 3. Intensity and time course of the weight loss were correlated to the morphine treatment. 4. On the other hand, the morphine-treated rats showed abnormal behaviors, such as diarrhea, ptosis, teeth chattering, salivation, body shakes, vocalization, nose bleed, irritability, aggression, lacrimation and writhing upon naloxone injection. 5. Loss of body weight, measured 3 hours after naloxone injection, was also correlated to the duration of morphine treatment. 6. Tolerance to the analgesic effect of morphine developed within one day in rats treated with morphine-admixed food. 7. The drug-admixed food ingestion method has the advantage of rapidly inducing a high degree of physical dependence and tolerance without causing morbidity or lethality in animals. It also eliminates the need for excessive handling of animals.
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PMID:Development of physical dependence on and tolerance to morphine in rats treated with morphine-admixed food. 668 88

Various drugs acting on brain serotonin or catecholamines were administered concurrently with morphine during the development of dependence or before naloxone-precipitated withdrawal syndrome. Of the various drugs only cyproheptadine, a serotonin antagonist, and piribedil, a dopamine agonist, reduced the frequency of jumping (but not of diarrhea or ptosis) when administered with morphine during development of dependence. When administered before naloxone, d-fenfluramine, a serotonin releaser, markedly reduced jumping, but not diarrhea and ptosis, and clonidine blocked these latter signs without affecting the frequency of jumping. Of the other drugs examined only phenoxybenzamine reduced diarrhea in morphine-abstinent rats. It is suggested that serotonin is involved in the mechanisms which lead to compulsive jumping during naloxone-precipitated withdrawal, whereas adrenergic sites on which clonidine acts are mainly involved in the expression of signs, such as ptosis and diarrhea. No clear evidence was obtained of a role for dopamine in the withdrawal signs studied.
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PMID:Evidence of a preferential role of brain serotonin in the mechanisms leading to naloxone-precipitated compulsive jumping in morphine-dependent rats. 679 Dec 37

Ninety-five patients have been referred for the assessment and treatment of faecal incontinence. Incontinence was associated with previous anal trauma in 49 cases: 13 occurred after vaginal delivery, 32 were associated with anal operations and in 4 severe perineal trauma occurred after road accidents. Other causes were: idiopathic incontinence in 18, persistent incontinence despite successful rectopexy for prolapse in 10, diabetic neuropathy in 5 and in 13 the cause was not identified. Conservative treatment by control of diarrhoea, physiotherapy or electrical therapy was often successful in patients with minor incontinence. Fifty-six patients have been treated surgically. Complete continence was achieved in 67 per cent of patients treated by postanal repair and in 61 per cent by sphincter reconstruction. We believe that postanal repair is the treatment of choice for idiopathic incontinence and incontinence after rectopexy or anal dilatation. Sphincter repair should only be performed with a covering colostomy and is the treatment of choice for recent or long standing division of the external sphincter ring.
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PMID:Management of faecal incontinence and results of surgical treatment. 687 36

Fifty-six patients were treated for rectal prolapse or incontinence. Rectal prolapse was present in 32 patients and was associated with fecal incontinence in 24 (75 per cent). Incontinence without prolapse was present in 24 patients, 12 of whom were less than 40 years old. Rectopexy was used for treatment of rectal prolapse. Surgical treatment of fecal incontinence was by postanal repair; external sphincter reconstruction and surgery was advised only if control of diarrhea and electrical therapy had been of no benefit. Rectopexy was completely successful at controlling rectal prolapse in all cases, and only four of the 20 (20 per cent) patients with incontinence and prolapse remained incontinent after rectopexy alone. Incontinence was completely controlled by postanal repair in 58 per cent of patients and by external sphincter repair alone or in combination with postanal repair in 67 per cent. Using a combination of therapies 45 of 48 patients who were initially incontinent were improved (94 per cent), and 42 of the patients have complete control of defecation (87 per cent).
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PMID:Results of treatment for rectal prolapse and fecal incontinence. 702 89

The effects of the normotensive, mainly centrally active nitric oxide synthase (NOS) inhibitor 7-nitro indazole and the hypertensive drug NG-nitro-L-arginine, which blocks both the endothelial and the central NOS, have been examined on naloxone-precipitated withdrawal in morphine-dependent rats. Both drugs attenuated the same withdrawal signs (teeth-chattering, penile licking, diarrhoea, chewing, wet-dog shakes, grooming), while other signs remained unaffected (rearing, jumping, ptosis, rhinorrhoea, irritability on touch). These findings indicate that mainly central (but not endothelial) nitric oxide is involved in the expression of some opioid withdrawal symptoms.
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PMID:Comparative study of normotensive and hypertensive nitric oxide synthase inhibitors on morphine withdrawal syndrome in rats. 753 10

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


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