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Query: UMLS:C0278080 (physical dependence)
 1,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A slow release emulsion of naloxone (naloxone SR) was administered subcutaneously to rats in an attempt to induce physical dependence of the morphine type. 2. Naltrexone (2.5 mg/kg), injected i.p., failed to elicit an abstinence syndrome in rats treated with 75, 100 or 150 mg/kg naloxone SR for 24, 48, or 72 h. 3. Naloxone SR had no effect on the whole brain levels of noradrenaline, dopamine, homovanillic acid or serotonin. 4. Naloxone SR caused an apparent dose-related increase in the brain levels of 5-hydroxyindoleacetic acid. 5. These results show that while naloxone does not induce physical dependence of the morphine type, it may, like morphine, increase the brain serotonin turnover rate. 6. It is proposed that the increase in brain serotonin turnover rate may not be causally related to physical dependence on morphine-like drugs but may be a property of drugs containing the basic opiate molecular structure.
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PMID:Dissociation of increased 5-hydroxyindoleacetic acid levels and physical dependence: the effects of naloxone. 56 13

Rats were treated for 24, 48 or 72 h with slow release (SR) emulsions of morphine (75, 100 and 150 mg/kg), cyclazocine (75, 100 and 150 mg/kg) or pentazocine (100, 200 and 400 mg/kg). At these times the degree of physical dependence was assessed by examining the abstinence behavior (jumps + wet shakes), changes in body temperature and body weight induced by naloxone (5 mg/kg). The effects of SR treatments on brain levels of noradrenaline (NA), dopamine (DA), homovanillic acid (HVA), 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were also determined at these times. The results show that all three opiates induce physical dependence in the order of severity of morphine greater than cyclazocine greater than pentazocine. An elevation of 5-HT turnover also appears to be associated with the dependence produced by these opiates. These findings indicate that the increase in brain 5-HT metabolism is not a primary causative factor during opiate dependence, but occurs in response to some other process.
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PMID:Induction of physical dependence on cyclazocine and pentazocine in the rat. 56 89

Rats were fed on liquid diets containing ethanol or t-butanol. On removal of either alcohol from the diet after 4-20 days, withdrawal reactions were observed. The range of withdrawal signs produced by the two alcohols were identical although the time course of the withdrawal reactions differed. Administration of one alcohol prevented the appearance of a withdrawal reaction in rats dependent on the other alcohol. Depletion of brain noradrenaline and dopamine did not prevent the development of physical dependence on either alcohol. Thus, neither aldehyde formation nor brain catecholamines appear to be involved in the development of physical dependence on these alcohols.
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PMID:Physical dependence following prolonged ethanol or t-butanol administration to rats. 57 6

1. Physical dependence was induced in rats by administration of a slow release morphine emulsion (morphine SR), and assessed by scoring abstinence signs and temperature changes after i.p. administration of naloxone (5 mg/kg). Three groups of rats received doses of 75, 100 or 150 mg/kg of morphine SR. Dependence was evaluated in each of these groups after 24, 48 and 72 h. 2. The effect of these treatments at the different times on brain levels of serotonin, 5-hydroxyindoleacetic acid, noradrenaline and dopamine was determined. 3. A ceiling level of dependence was reached 24 h after 75 and 100 mg/kg and 48 h after 150 mg/kg of morphine SR. 4. These different treatments produced no significant effect on the brain levels of noradrenaline, dopamine or serotonin. The levels of 5-hydroxyindoleacetic acid were significantly raised in morphine-dependent rats and the changes correlated well with the changes in abstinence behaviour and temperature after naloxone. 5. The results suggest that a relationship exists between serotonin turnover and physical dependence on morphine.
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PMID:Physical dependence in the rat induced by slow release morphine: dose-response, time course and brain biogenic amines. 103 33

Adrenaline and noradrenaline levels in the adrenal glands and the excretion of both bioamines in urine of adult cats were investigated after chronic administration of morphine and nalorphine-induced withdrawal. After 7 days of daily consecutive morphine treatment, a significant increase in the adrenal noradrenaline content and a drop in adrenaline content were observed. After 2 weeks of daily injection of morphine, no significant changes were observed in the adrenal catecholamine level. One month of treatment with the opioid caused a significant increase in the adrenal content of both adrenaline and noradrenaline. Urinary excretion of catecholamines was significantly increased during the 4 weeks of treatment. In animals subjected to spontaneous or induced withdrawal with nalorphine, the adrenal content of catecholamines was altered and the ratio adrenaline/noradrenaline in the adrenal gland was shifted towards noradrenaline. A first injection of morphine produced an excitant manic response characterized by hyperexcitement and aggressive behaviour; animals chronically treated with the drug showed a progressively diminished response to this effect of the drug. It is concluded that physical dependence on morphine is reached by cats chronically treated with morphine and that this effect of the drug influences adrenomedulllary function in a different fashion depending on the stage of morphine treatment.
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PMID:Chronic administration of morphine in cats: effects on adrenal and urinary catecholamines. 117 Oct 18

Although p.o. self-administration of morphine is a reliable and convenient means of inducing physical dependence, its effects on brain monoamine metabolism have not been determined. Accordingly, in the present experiment young Wistar rats drank increasing concentrations (0.1-0.5 mg/ml) of morphine in water, or water alone, for 37 days. Half the rats in each group were challenged with morphine (10 mg/kg s.c.) when 27 to 29 hr withdrawn, and half with saline. Rats were sacrificed 2 hr postinjection. Seven brain regions were analyzed for noradrenaline (NA), dopamine (DA), or 5-hydroxytryptamine (5-HT), and their respective metabolites. In all cases in which a comparison could be made with prior work utilizing repeated injections to produce dependence, the p.o. regimen produced the same effects. Thus, the mode of administration does not seem to modify the response of monoaminergic neurons to chronic morphine. In withdrawal, NA turnover increased but DA and 5-HT turnovers decreased. Acute morphine accelerated the turnover of all three monoamines. The NA response was attenuated in some brain regions of withdrawn rats, indicating the development of tolerance to the turnover-enhancing effect of acute morphine in noradrenergic neurons. In contrast, the effect of acute morphine on cerebral 5-HT turnover was not altered, and its effect on cerebral DA turnover was enhanced in withdrawn rats. Our results suggest that there are fundamental differences among the three monoaminergic systems in their capacities for adapting to chronic morphine treatment.
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PMID:Changes in brain monoamine metabolism during withdrawal from chronic oral self-administration of morphine and in response to a morphine challenge in the withdrawn state. 246 63

Changes in the noradrenaline (NA) content in the hypothalamus, dopamine (DA) and homovanillic acid (HVA) in the striatum were determined in rats after chronic alcohol administration. A single injection of alcohol (2.5 g/kg i.p.) provoked a 30% decrease in NA only in rats predisposed to ethanol intake. Voluntary intake of 15% ethanol for 10 days made the NA content return to normal, the 4-month use of ethanol did not change whereas the 8-month use reduced the NA content by 17%, DA by 31% and raised the content of HVA by 25%. Twenty-four hours after alcohol abstinence the HVA content dropped by 13%. It is concluded that the noradrenergic system is involved in the formation and development of alcohol motivation and that the dopaminergic system participates in the development of the physical dependence and abstinence.
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PMID:[Catecholamine content of the rat brain at different stages of experimental alcoholism]. 403 98

The effects of clomipramine HCl (15 mg kg-1 i.p.) on behaviour, body temperature and brain amines were investigated in rats that had been chronically treated twice daily with increasing doses of delta 9-tetrahydrocannabinol (delta 9-THC, 2-6 mg kg-1 i.v.). delta 9-THC produced a biphasic change in behaviour, stimulation followed by depression, and a pronounced hypothermia. Tolerance developed rapidly to these effects of delta 9-THC. Chronic treatment with delta 9-THC reduced the levels of homovanillic acid, 5-hydroxytryptamine and noradrenaline. The level of dopamine was not altered with chronic treatment and tolerance appeared to develop to the increased levels of 5-hydroxyindoleacetic acid induced by delta 9-THC. Injection of clomipramine, 12-14 h after 2, 5 or 10 days of delta 9-THC treatment induced characteristic changes in the rats behaviour which consisted of writhes, backward kicking, wet shakes, jumps ataxia and front paw and whole body tremor. The severity of the behavioural changes appeared to be dependent on the period of delta 9-THC administration and they were not accompanied by a change in body temperature or consistent changes in brain amines or metabolites. The results indicate that physical dependence on delta 9-THC may occur since clomipramine is able to precipitate changes in behaviour, indicative on an abstinence syndrome, in rats chronically treated with delta 9-THC. It is suggested that tryptaminergic mechanisms are altered during chronic delta 9-THC treatment and that clomipramine induces the behavioural changes by interacting with an altered tryptaminergic system.
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PMID:Time-course of the effects of chronic delta 9-tetrahydrocannabinol on behaviour, body temperature, brain amines and withdrawal-like behaviour in the rat. 612 98

1. The half-time for maximal withdrawal scores in the rat is 30 to 36 hours following around the clock intubation with ethanol. 2. Cyclic AMP levels in all brain areas decline with ethanol treatment and rise again to control levels during withdrawal. 3. Norepinephrine-stimulated adenylate cyclase activity is increased by chronic treatment with ethanol. However, it is unlikely that this change is related to physical dependence, as it occurs 50 to 60 hours following the development of half-maximal withdrawal scores. 4. Ethanol had no effect on the concentration of beta-receptors in the cerebral cortex.
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PMID:Cyclic AMP and beta-adrenergic receptors during the development of physical dependence on ethanol in the rat. 625 Mar 27

The effect of pretreatment with a delta opioid receptor antagonist, naltrindole (NTI), on the development of physical dependence on morphine was investigated in mice. Several withdrawal signs, an increase in cortical noradrenaline (NA) turnover and a decrease in dopamine (DA) turnover in the limbic forebrain were observed following naloxone challenge in morphine-dependent mice. Pretreatment with NTI (0.3-5 mg/kg, s.c.) during chronic morphine treatment dose-dependently suppressed the behavioral and biochemical changes after withdrawal. The blocking effects of NTI suggest that delta opioid receptors may play a significant role in modulating the development of physical dependence on morphine.
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PMID:Effect of naltrindole on the development of physical dependence on morphine in mice: a behavioral and biochemical study. 756 99


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