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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 76 (1982), S. 114-117 
    ISSN: 1432-2072
    Keywords: Brain ; β-Adrenoceptors ; Serotonin synthesis ; Metoprolol ; ICI 118,551 ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rats were treated subchronically (14 days) or acutely (single dose) with the β1-selective adrenoceptor antagonist metoprolol or the β2-selective adrenoceptor antagonist ICI 118,551. Metoprolol (350 mg/kg/day for 14 days, orally) significantly reduced the 5-hydroxytryptophan (5-HTP) accumulation when measured 30 min after inhibition of L-amino acid decarboxylase by NSD 1015 (100 mg/kg IP) in the limbic forebrain, the corpus striatum, the cerebral cortex, the brain stem, and in the cerebellum. ICI 118,551 (0.5 mg/kg, twice daily for 14 days, SC) also significantly reduced the 5-HTP accumulation in the same brain regions except in the corpus striatum and the brain stem. Simultaneously assayed tryptophan levels were largely unaffected. Thus sustained β-adrenoceptor blockade causes a decrease in the in vivo rate of tryptophan hydroxylation in various rat brain regions. The subchronic treatments with metoprolol or ICI 118,551 also significantly reduced the endogenous levels of 5-hydroxytryptamine (5-HT) in the various rat brain regions studied. Acute treatment with either metoprolol (2 mg/kg SC) or ICI 118,551 (0.5 mg/kg SC) did not affect the 5-HTP accumulation or the endogenous 5-HT levels in the brain regions studied. This inhibitory effect on brain 5-HT systems produced by sustained β-adrenoceptor blockade may be of significance both for the long-term cardiovascular action and for occasional neuropsychiatric side effects during β-blocking therapy.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Beta-2-receptor agonist ; Salbutamol ; Monoamine synthesis ; Serotonin ; Noradrenaline ; Dopamine ; Antidepressant
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Subchronic (5 mg/kg SC, twice daily for 14 days) but not acute administration of the beta-2-adrenoceptor agonist salbutamol to rats caused a significant increase in the accumulation of 5-hydroxytryptophan in the limbic forebrain, the corpus striatum and the cerebral cortex when measured during 30 min after inhibition of l-amino acid decarboxylase by NSD 1015 (100 mg/kg IP). Simultaneously assayed tryptophan concentrations in the same brain regions were not affected. These results indicate an increase in the in vivo rate of tryptophan hydroxylation in the brain, produced by subchronic salbutamol administration. The effect of salbutamol treatment on brain catecholamine (CA) utilization was estimated by studying the disappearance of CA in the brain after inhibition of tyrosine hydroxylase by alpha-methyltyrosine methyl ester (H 44/68) 250 mg/kg IP, 3.5 h before sacrifice. Subchronically but not acutely administered salbutamol caused both a significant increase in endogenous noradrenaline (NA) levels and an increased NA utilization. Dopamine levels and turnover were, however, not altered by either acute or subchronic treatment. The activation, probably centrally elicited, of brain NA and 5-hydroxytryptamine systems by the subchronic salbutamol regimen supports the concept of beta-adrenoceptor mediated regulation of brain monoamine systems, and could contribute to the clinically reported antidepressant activity of beta-2-adrenoceptor agonists.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2072
    Keywords: Beta-adrenoceptors ; Locomotor activity ; Propranolol ; Apomorphine ; Clonidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was undertaken in order to clarify the possible involvement of a central betaadrenoceptor mediated action on the stimulation of locomotor activity by the dopamine agonist apomorphine and the noradrenergic agonist clonidine. The effect of pretreatment with various doses of d-and dl-propranolol on apomorphine- and apomorphine plus clonidine-induced locomotor stimulation in reserpinized mice was measured in photocell activity chambers. Pretreatment with dl-propranolol prolonged the duration of apomorphine-induced locomotor stimulation without affecting the maximal level of activity. A similar tendency was seen after pretreatment with the d-form of propranolol, which has a much lower beta-receptor blocking activity. The potentiation by clonidine of the apomorphine-induced locomotor stimulation in reserpinized mice was dose-dependently reduced by pretreatment with dl-propranolol whereas d-propranolol was found to be ineffective. The results indicate that central beta-receptor mechanisms might be involved in the apomorphine plus clonidine-induced locomotor stimulation of reserpinized mice.
    Type of Medium: Electronic Resource
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