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  • Dopamine  (2)
  • Midbrain Raphe  (2)
  • Withdrawal syndrome  (2)
  • 1
    ISSN: 1432-2072
    Keywords: Morphine dependence development ; Withdrawal syndrome ; Monoamine agonist ; Monoamine antagonist
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Various drugs acting on brain serotonin or catecholamines were administered concurrently with morphine during the development of dependence or before naloxoneprecipitated 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 naloxoneprecipitated 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.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Buspirone ; Haloperidol ; Sulpiride ; Anxiolytics ; Punished responding ; Dopamine ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Low doses of buspirone, haloperidol and sulpiride were compared with diazepam in two experimental models of anxiety in rats. In a conflict test, 0.6 and 1.2 mg/kg buspirone, 0.05 and 0.10 mg/kg haloperidol and 0.5 mg/kg sulpiride significantly increased punished responding. Buspirone 1.2 and 2.5 mg/kg significantly reduced the number of unpunished responses while haloperidol and sulpiride at the doses tested had no effect. Effects on punished responding were seen in a narrow dose range and were less pronounced with these drugs than with diazepam. Similar results were obtained with rats', activity in the two-compartment exploratory test. At doses causing no change in the locomotion of rats in photocell activity cages, buspirone (0.1 mg/kg), haloperidol (0.025–0.100 mg/kg) and sulpiride (0.5–1.0 mg/kg) significantly increased the number of crossings between the two compartments. Again, the peak effects were small when compared with the effect of diazepam and the active dose range was very narrow. Apomorphine 0.2 mg/kg SC significantly counteracted the effect of 0.1 mg buspirone and 1.0 mg/kg sulpiride in the two-compartment exploratory test with no effect on 2.5 mg/kg diazepam. The data show that buspirone, in a narrow dose range, shows disinhibitory effects in experimental models of anxiety. Similar effects are shown by low doses of haloperidol and sulpiride. It is suggested that buspirone and sulpiride produce these disinhibitory effects by blocking particular dopamine receptors in the brain, possibly those located in the nerve terminals, but it is likely that other mechanisms, particularly serotonin, are involved in the effects of buspirone in anxious states.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2072
    Keywords: Morphine dependence ; Withdrawal syndrome ; Locus coeruleus ; Norepinephrine, clonidine ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Naloxone HCl (10 μg/0.5 ml) was injected in the locus coeruleus (LC) of morphine-dependent rats and the behavioural manifestations of morphine withdrawal and the cortical levels of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) were measured 30 min later. Naloxone precipitated a withdrawal syndrome and raised cortical MHPG-SO4 in animals made dependent by ascending doses of morphine for 11 days. An injection of clonidine intraperitoneally (200 μg/kg) or in the LC (5 μg/0.5 μl) blocked most aspects of the withdrawal syndrome except jumping and had no effect on the naloxone-induced rise in cortical MHPG-SO4. The findings confirm the hypothesis that the LC is one of the sites where naloxone and clonidine, respectively, precipitate and reduce the narcotic withdrawal syndrome but argue against a role of noradrenergic neurons originating in the LC and innervating the cortex in the ability of clonidine to suppress some aspects of withdrawal syndrome precipitated by naloxone in morphine-dependent animals.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2072
    Keywords: Neurotensin ; Dopamine ; Mesolimbic system ; Antidepressant activity ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Locomotor activity and behaviour in the forced swimming test were examined in rats which had received neurotensin (0.5–5.0 µg) in the ventral tegmental area. Doses of 5 µg neurotensin but not lower increased the locomotor activity for at least 2 h. At 0.5 and 1.0 µg neurotensin significantly increased the time the animals spent in struggling with no changes in general motor activity (swimming). The effect of 1.0 µg neurotensin on struggling was completely antagonized by 0.5 µg (−)-sulpiride administered in the posterior nucleus accumbens. The results suggest that activation of the mesolimbic dopamine system through administration of neurotensin in the ventral tegmental area produces antidepressant-like effects. The significance of these findings for a role of endogenous neurotensin in depression remains to be clarified.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 25 (1972), S. 175-182 
    ISSN: 1432-2072
    Keywords: 6-OH Dopamine ; Midbrain Raphe ; Serotonin ; Catecholamines ; Morphine Analgesia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two different techniques were employed to measure morphine analgesia, the hot-plate and the tail compression. An intraventricular injection of 6-hydroxydopamine, which produced a marked decrease of brain noradrenaline and dopamine, strongly potentiated the analgesic effect of morphine. The lesion of midbrain raphe, which lowers forebrain serotonin, antagonized morphine analgesia. 5-Hydroxytryptophan restored serotonin levels and the analgesic effect of morphine in midbrain raphe lesioned rats. The role of brain serotonin and catecholamines on morphine analgesia is discussed.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 24 (1972), S. 373-379 
    ISSN: 1432-2072
    Keywords: Midbrain Raphe ; Stimulation ; Evoked Potentials ; Sensory Cortex ; Strychnine ; Picrotoxine ; LSD25
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stimulation of the midbrain raphe (MR) area in rats induced a decrease of the peripherally evoked potentials in the primary sensory cortex. The inhibition was blocked by relatively small doses of strychnine whereas picrotoxine was ineffective. Low doses of LSD25, markedly potentiate the effect of MR stimulation.
    Type of Medium: Electronic Resource
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