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  • 1
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of medicinal chemistry 33 (1990), S. 1541-1544 
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1912
    Keywords: Dopamine ; Axotomy ; Gammahydroxybutyric Acid ; Receptor Activity ; Amphetamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of blockade or stimulation of dopamine (DA) receptors on the selective increase in brain DA seen after axotomy or injection of gammahydroxybutyric acid (sodium form, 1.5 g/kg i.p.) was studied in rats. The increases were not changed after blockade of the DA receptors by haloperidol but were slightly reduced after stimulation of these receptors by apomorphine. Since pretreatment with haloperidol counteracted this effect of apomorphine, a diminished stimulation of DA receptors may partially be responsible for the increase in brain DA seen when the nerve impulse flow has been blocked in the DA neurones by axotomy or treatment with gammahydroxybutyric acid. The NA content was usually somewhat lowered on the lesioned side and this reduction was not changed after treatment with haloperidol, apomorphine or amphetamine. The increase in brain DA usually observed after axotomy was not found when the rats were also treated with reserpine and nialamide. This effect indicates that the negative feed-back of cytoplasmic DA on the DA synthesis operates also in the absence of nerve impulses. Injection of amphetamine before or after axotomy or treatment with gammahydroxybytyric acid markedly inhibited the increase in brain DA, probably due to release of newly synthesized DA.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 273 (1972), S. 1-10 
    ISSN: 1432-1912
    Keywords: l-DOPA ; Central Noradrenaline Receptors ; Receptor Stimulation ; Noradrenaline Release ; Tachyphylaxis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Changes in central noradrenaline receptor activity were correlated with changes in dopamine and noradrenaline concentrations in rats after treatment with l-3,4-dihydroxyphenylalanine (l-DOPA) in combination with different drugs. The noradrenaline receptor activity was tested by means of flexor reflex increase and blood pressure reduction. After depletion of the endogenous noradrenaline stores by reserpine, and inhibition of the monoamine oxidase by nialamide, the l-DOPA treatment produced increases in flexor reflex activity and in both dopamine and noradrenaline concentrations. Pretreatment with the dopamine-β-hydroxylase inhibitor FLA-63 revealed that both catecholamines were of importance for this functional effect. Without monoamine oxidase inhibition, the administration of l-DOPA (after inhibition of the peripheral l-DOPA decarboxylase by l-α-methyldopa hydrazine) did not cause any functional effect, despite almost the same accumulation of dopamine. Injection of l-DOPA (after inhibition of the peripheral decarboxylase) into rats with intact noradrenaline stores evoked increased flexor reflex activity concomitant with a small but significant disappearance of noradrenaline and reduced the mean arterial blood pressure by 24–35 mm Hg. A second dose of l-DOPA had a much smaller effect on flexor reflex activity and on blood pressure, when given 90 min–12 h after the first one. This tachyphylaxis coincided with a fractional loss of endogenous noradrenaline and was not due to desensitization of the effector cells. In conclusion, the dopamine and noradrenaline formed from l-DOPA after monoamine oxidase inhibition act directly on the central noradrenaline receptors. Without monoamine oxidase inhibition, the l-DOPA treatment elicits a central noradrenaline receptor activation via release of endogenous noradrenaline, presumably by displacement of a small noradrenaline store with dopamine.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 333 (1986), S. 17-22 
    ISSN: 1432-1912
    Keywords: Dopamine ; Noradrenaline ; Sympathetic ganglion ; Nicotine receptors ; Muscarine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Electrical stimulation of the preganglionic sympathetic neurons rapidly and markedly elevated the contents of the primary dopamine (DA) and noradrenaline (NA) metabolites, i.e., 3,4-dihydroxyphenylacetic acid (DOPAC) and 3,4-dihydroxyphenylethylene glycol (DOPEG) in the superior cervical ganglion and it enhanced the accumulation of DOPAC and DA following inhibition of the DA-β-hydroxylase by FLA-63. The stimulation also increased the concentration of DA and decreased the concentration of NA in the salivary gland both without and with DA-β-hydroxylase inhibition. Chlorisondamine inhibited the increase in ganglionic DOPAC following preganglionic stimulation (5 Hz, 30 min) by 30–50% and it even better reduced the biochemical changes in the salivary gland. Atropine did not produce any clearcut inhibition of the stimulation-induced effects on the superior cervical ganglion or the salivary gland, nor did it enhance the effect of chlorisondamine. The results suggest that nicotine, but not muscarine receptors in the cell body region of the postganglionic NA neurons partially mediate the effects of preganglionic stimulation. The effects remaining after blockade of the nicotine and muscarine receptors might be due to release of a neuropeptide acting on a special receptor. The stimulation-induced increase in the concentration of DOPAC in the superior cervical ganglion might, at least partly, be the result of a depolarization of the NA nerve cell body regions since similar changes were produced by electrical stimulation of the chronically decentralized ganglion.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 278 (1973), S. 347-361 
    ISSN: 1432-1912
    Keywords: Dopamine ; Noradrenaline ; Nerve Impulses ; Hemisection ; Gammaydroxybutyric Acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Both a unilateral, frontal section of the brain at the level of the caudal hypothalamus (hemisection) and systemic treatment with gammahydroxybutyric acid (GHBA, sodium form, 1.5 g/kg i.p.) increased the dopamine (DA) in the rat forebrain by about 70% in 1 h. Both procedures also markedly decelerated the α-methyltyrosine-induced DA disappearance. The brain noradrenaline was significantly lowered after the hemisection, but was not influenced by the treatment with GHBA given either alone or in combination with α-methyltyrosine. Intrastriatal injections of 25% KCl did not change the normal DA content significantly but prevented the increase in DA observed after hemisection or treatment with GHBA, probably due to a depolarization of the DA nerve terminals. Such a treatment with KCl also rapidly released the DA accumulated after hemisection. These effects were not seen after 20% NaCl. The same increase in forebrain DA, as produced by hemisection or treatment with GHBA, was also seen after injections of 25% KCl into the substantia nigra or injections of tetrodotoxin into the neostriatum. To judge from the turning of rats, unilateral injections of 25% KCl into the neostriatum depolarized the cells in this area, whereas stimulation of the DA receptors hyperpolarized them. The increases in brain DA described may be due to an inhibition of the nerve impulse flow to the DA nerve terminals.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 273 (1972), S. 11-26 
    ISSN: 1432-1912
    Keywords: DOPA Uptake ; DOPA Decarboxylation ; Noradrenaline Receptor Stimulation ; Capillary Walls ; Nerve Terminals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The uptake and decarboxylation of 3,4-dihydroxyphenylalanine (DOPA) in the central nervous system were studied in spinal rats. The neuronal l-DOPA decarboxylase can be eliminated in the spinal cord caudal to a chronic (9–15 days) transection. The DOPA decarboxylase in the periphery and in the central capillary walls, but not in the central neurons, can be inhibited by l-α-methyl-dopa hydrazine (αMDH, 100 mg/kg i.p.). The DOPA-induced noradrenaline receptor stimulation in the caudal part of the spinal cord was studied by determining increase in hindlimb flexor reflex activity. No marked central accumulation of DOPA was observed after injection of the d-isomer, demonstrating a barrier for the passage of DOPA from the blood. l-DOPA was taken up by a stereoselective mechanism. Pretreatment with αMDH increased the central tissues to plasma ratio of the concentrations of l-DOPA, indicating that there is also an enzymatic barrier for l-DOPA in the capillary walls. After treatment with l-DOPA, no formation of noradrenaline was noted in the spinal cord caudal to a chronic transection because of the disappearance of the noradrenaline nerve terminals with their dopamine-β-hydroxylase activity. The l-DOPA-induced dopamine accumulation in the spinal cord was not reduced caudal to a chronic transection, indicating that most of the l-DOPA entering the central nervous system was decarboxylated in the capillary walls. The dopamine synthesized in the chronically transected cords presumably diffused from the capillary walls to the (probably supersensitive) noradrenaline receptors and produced the same effect as the dopamine and noradrenaline coming from the nerve terminals in the acutely transected cords. In the chronically transected spinal cords, αMDH inhibited the dopamine formation from l-DOPA because of interference with the capillary decarboxylase. In the acutely transected spinal cord, pretreatment with αMDH did not change the amount of dopamine synthesized from l-DOPA, i.e., the decarboxylation occurred in the monoamine nerve terminals instead of in the capillary walls.
    Type of Medium: Electronic Resource
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