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  • 1
    ISSN: 1432-2072
    Keywords: Morphine-6-Hydroxydopamine ; Analgesia ; Brain Catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract One week following the intraventricular administration on successive days of two doses of 6-hydroxydopamine (6-OHDA) (0.1–1 mg/kg) to rats, the norepinephrine (NE) and dopamine (DA) contents in the brain were markedly decreased. These treatments potentiated the effect of morphine on the tail-flick latency after intraperitoneal or intraventricular administration of morphine. The intraventricular administration of two doses of 6-OHDA (0.5 mg/ kg) did not change the morphine concentrations in brain or plasma, or the duration of pentobarbital anesthesia. After 6-OHDA (total=20 Μg) had been injected bilaterally into the medial hypothalamic areas at the level of the ventromedial or dorsomedial hypothalamic nuclei, or into the medial forebrain bundle, morphine analgesia was also potentiated and there was marked reduction of the hypothalamic NE levels. The administration of high doses (2 mg/kg) of 6-OHDA into the lateral ventricles decreased the enhanced morphine analgesia and markedly depleted the brain NE and dopamine concentrations. The administration bilaterally of 6-OHDA (total=20 Μg) into caudatus-putamen areas reduced morphine analgesia. In conclusion, 6-OHDA induced depletion of NE content in the hypothalamus potentiates morphine analgesia, whereas depletion of DA in the caudate nucleus decreases morphine analgesia.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Intraventricular 6-Hydroxydopamine ; Increased Irritability ; Norepinephrine Turnover ; Benzodiazepines ; Neuroleptics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intraventricular injection of 2 doses of 300 μg of 6-hydroxydopamine (6-OHDA) into rats induced an increased reactivity to exogenous (non-painful) stimuli. This increased irritability lasted more than 4 months (the longest period studied) and consisted of crying, hissing, urination, defecation, standing in an upright posture, biting and panic jumping. The degree of irritability was inversely correlated with the level of brain norepinephrine (NE). The uptake of 3H-NE into all brain regions studied was decreased after administration of 6-OHDA. The rate of 3H-NE decay from the brain stem (hypothalamus, medulla-pons) was delayed 1 week and accelerated 9 weeks after 6-OHDA administration. The decay of 3H-NE from the residual parts of the brain was enhanced both 1 and 9 weeks after 6-OHDA injection. Diazepam, chlordiazepoxide and meprobamate suppressed the increased irritability at doses which did not cause muscle relaxation. The normalization of the behavior produced by diazepam was accompanied by a normalization of the rate of 3H-NE decay both in the brain stem and the residual parts of the brain. The neuroleptics chlorpromazine and haloperidol were effective in abolishing the increased irritability only at strongly sedative doses.
    Type of Medium: Electronic Resource
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