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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 41 (1983), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A gas chromatographic-mass spectrometric assay, which allowed simultaneous measurement of 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenylglycol (DHPG), was used to show that the concentration of MHPG in primate CNS far exceeded that of DHPG and that both metabolites were mainly in the unconjugated form. In rat brain, DHPG concentration was generally higher than that of MHPG, and both existed predominantly as conjugates. Rat and primate plasma contained more MHPG than DHPG. In plasma of primates but not of rats, higher proportions of the metabolites were conjugated, compared to those in brain. Significant correlations existed between MHPG and DHPG in rat brain, monkey brain, human plasma, and both monkey CSF and plasma. In monkeys, a significant CSF-plasma correlation was found for MHPG, but not for DHPG. Acute administration of piperoxane raised rat brain MHPG and DHPG concentration; desipramine prevented this rise in DHPG, but not in MHPG. Desipramine alone decreased DHPG, but not MHPG, concentration. Piperoxane increased monkey brain MHPG, but not DHPG, concentration. These data suggest that DHPG is a valuable metabolite to measure when assessing norepinephrine metabolism in the rat. Under certain conditions, measurement of rat brain MHPG and DHPG may provide information concerning the site of norepinephrine metabolism. However, in primates the importance of monitoring DHPG, in addition to MHPG, is uncertain.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 32 (1979), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— The concentration of dopamine (DA) and serotonin (5-HT) metabolites in brain regions was not altered by doses of ketamine (10mg/kg) which induced dissociative anesthesia in a primate species. Cercopithecus aethiops. Fluphenazine (1.0mg/kg) increased homovanillic acid (HVA) content in all brain regions examined. An increase in HVA and 5-hydroxyindoleacetic acid (5-HIAA) concentration was observed in cisternal CSF 4 h after ketamine without a concomitant change in the brain concentration of these metabolites.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Neuroscience 7 (1984), S. 443-478 
    ISSN: 0147-006X
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 495 (1987), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1435-1463
    Keywords: Homovanillic acid ; frontal cortex ; striatum ; cerebrospinal fluid ; plasma ; primate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a large number (91) of vervet monkeys, correlation coefficients were determined between homovanillic acid (HVA) concentrations in four brain areas. Significant correlations existed between dorsal frontal cortex and orbital frontal cortex and between putamen and caudate nucleus. However, no significant correlations existed between either cortical area and the basal ganglia areas. Correlations were tested between CSF and plasma HVA and between these fluids and brain regions. The only significant relationship found was between CSF and dorsal frontal cortex, after possible treatment effects were statistically removed. The assumption that primate CSF HVA concentration necessarily reflects basal ganglia HVA concentration is questioned and furthermore, the results suggest that HVA from cortex contributes significantly to that in cisternal CSF. Raw plasma HVA measurements (even when uninfluenced by diet or anesthetic) appear to be of limited value in gauging central dopamine metabolism and turnover.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1106
    Keywords: MPTP ; Graft ; Behavior ; Parkinson's disease ; Monkey
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Fetal substantia nigra (SN) cells were transplanted into the caudate nucleus (CN) of four vervet monkeys (Cercopithecus aethiops sabaeus) that had been treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). MPTP treatment appears to produce a syndrome similar to that observed in patients with idiopathic Parkinson's disease. Normal and parkinsonian behaviors were quantitated by trained observers 5 days/week. Twenty-eight behaviors based on previous factor analyses were individually scored and rated. Parkinsonian signs included freezing, head and limb tremor, difficulty in eating, delayed initiation of movement, poverty of movement, tremor that stopped with intention, decreased response to threats, and lying immobile in the cage. These signs were combined to give an overall rating of parkinsonism. A summary measure of ‘normal’ healthy behavior was also examined, including such behaviors as yawning, scratching, self-grooming, shifting, and eating. Overall ratings of parkinsonism increased and those of healthy behavior decreased after MPTP. In the 4 monkeys grafted with fetal SN cells into the CN, behavior returned to pre-treatment levels by the time of sacrifice (2, 5, or 7.5 months after grafting). Three control subjects were transplanted with either SN cells into an inappropriate brain site (cortex) or inappropriate, non-dopaminergic, cells (cerebellar) into the CN. Subjects were also compared with three control animals that did not receive MPTP but received cryopreserved or fresh SN and other cells into the CN. Only MPTP-treated subjects that received SN cells into the CN showed evidence of a reversal of the MPTP syndrome after transplantation. In addition, grafting in animals that were not MPTP-treated did not appear to affect behavior. This paper reports the specific behavioral effects of severe MPTP toxicity that were or were not reversed after transplantation and suggests that only fetal SN cells grafted into the CN may be able to reverse behavioral deficits in MPTP-treated monkeys.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 32 (1976), S. 1213-1215 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Plasma amine oxidase activity increased from 23.4 nmol/ml/h during pregnancy to 49.5 nmol/ml/h during an extended post partum period in 10 rhesus monkeys. Comparison with non-pregnant control monkeys sampled at similar times indicated that the significant differences were in the extended post partum period.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-2072
    Keywords: Clonidine ; Locus coeruleus ; Intracerebral infusion ; Withdrawal ; Naloxone ; Morphine ; 3-Methoxy-4-hydroxyphenylglycol (MHPG) ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clonidine, an alpha-2-adrenergic agonist, suppresses signs of opiate withdrawal in animals and in man. Electrical or chemical stimulation of the nucleus locus coeruleus (LC) increases noradrenergic activity and brain concentration of the noradrenergic metabolite MHPG, and produces many signs of opiate withdrawal. Thus, clonidine's ability to attenuate withdrawal might be due to the reduction of noradrenergic neuronal activity originating in the LC, but additional alpha-2-adrenergic receptors throughout the body and other mechanisms may also play a role. The present study explored the neuroanatomical and pharmacological selectivity of alpha-2-adrenergic receptors of the LC in the anti-withdrawal action of clonidine. Experiment 1 tested the hypothesis that behavioral and biochemical measures of naloxone-precipitated withdrawal from morphine would be blocked by infusions of clonidine (0.6 or 2.4 μg/μl) into the LC. Significant reductions were observed in the occurrence of diarrhea, ptosis, weight loss and wet-dog shakes. Clonidine also reversed the naloxone-precipitated increase in hippocampus MHPG concentration. In experiment 2 subjects received an LC infusion or IP injection of a non-lipophilic alpha-2-agonist (ST-91), which does not penetrate the blood-brain barrier, or of clonidine into the dorsal parabrachial nucleus (DPB) to test the selectivity of the effects of clonidine infusions into the LC. ST-91 infusions into the LC reduced several of the observed withdrawal signs and increased others (e.g., jumping). Although peripheral injections of ST-91 attenuated some of the checked signs associated with naloxone-precipitated withdrawal, the frequency of wet-dog shakes was not reduced. ST-91 infusions into the LC, but not systemic ST-91 administration, prevented the withdrawal-induced increase in hippocampus MHPG concentration. Clonidine infused lateral to the LC into the DPB did not significantly attenuate withdrawal or reduce hippocampus MHPG levels. These results provide behavioral and biochemical evidence to support the suggestion that clonidine significantly attenuates naloxone-precipitated withdrawal through an interaction with noradrenergic neurons located in the vicinity of the LC.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-2072
    Keywords: Yohimbine ; Morphine ; Naloxone ; Withdrawal ; Tail flick latency ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Noradrenergic neuronal hyperactivity following chronic morphine administration has been postulated to cause withdrawal signs and symptoms. Suppression of this hyperactivity, for example, by clonidine attenuates withdrawal. It might follow, therefore, that the prevention of suppression of noradrenergic systems during chronic morphine administration might diminish hyperactivity and prevent withdrawal. If the normalization of noradrenergic activity during opioid administration did not also suppress analgesia, it might be of medical and theoretical interest. To test this hypothesis, we gave the alpha-2-antagonist yohimbine to rats in order to increase noradrenergic activity during morphine treatment and then subsequently precipitated morphine withdrawal with naloxone. Six groups were examined: saline controls (N=11), morphine (N=11), morphine + 2.0 mg/kg/day yohimbine (N=15), morphine + 3.0 mg/kg/day yohimbine (N=5), 2.0 mg/kg/day yohimbine (N=11) and 3.0 mg/kg/day yohimbine (N=5). Subjects received 75 mg morphine pellets implanted on day 1,4 and 6 of the treatment or sham implantation. Yohimbine was delivered throughout the morphine treatment by subcutaneously implanted osmotic pumps. On day 7, all subjects were given 1.0 mg/kg naloxone and rated for behavioral signs of withdrawal. Analgesia was measured by observing tail flick latencies (TFL) before and after chronic drug treatments. Naloxone-precipitated withdrawal was characterized by irritability, ptosis, penile erection, diarrhea, rhinorrhea, abnormal posture, wetdog shakes, jumping, and teeth chattering, none of which were observed in groups receiving only saline or yohimbine. Withdrawal behavior was attenuated in a dose-dependent manner when yohimbine was administered during morphine treatment but analgesia was not attenuated. It appears that yohimbine-induced antagonism of alpha-2-adrenergic receptors diminishes the development of the potential for adrenergic hyperactivity and morphine withdrawal without reducing opioid analgesia.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Monoamine oxidase in the vervet monkey showed greater variations in activity in six brain regions when tyramine or phenylethylamine was used as the substrate (3.8- to 4.1-fold differences) than when serotonin was the substrate (1.8-fold differences). With phenylethylamine and tyramine as substrates, the highest MAO specific activities were found in the hypothalamus and the lowest in the cerebellum and cortex. With serotonin as the substrate, the highest specific activities were in the mesencephalon and cortex. The inhibition of tyramine deamination by clorgyline and deprenyl yielded biphasic plots indicative of the presence of MAO-A and MAO-B enzyme forms in the vervet brain. On the basis of these inhibitor curves, the vervet brain could be estimated to contain approximately 85% MAO-B and 15% MAO-A, in contrast to rat brain which contains 45% MAO-B and 55% MAO-A. The inhibition of serotonin deamination by deprenyl in vervet brain yielded a biphasic plot, suggesting that some serotonin deamination in the vervet is accomplished by the MAO-B enzyme form. Estimations of the relative amounts of MAO-A and MAO-B based on inhibitor curves or based on substrate ratios yielded proportionate results which were in close agreement across the different brain regions, supporting the validity of these approaches to estimating MAO-A and MAO-B activities.
    Type of Medium: Electronic Resource
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