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  • 1
    Electronic Resource
    Electronic Resource
    Effects of drugs influencing monoamine mechanisms on the increase in brain dopamine produced by axotomy or treatment with gammahydroxybutyric acid (1973)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 278 (1973), S. 363-372 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00501480
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  • 2
    Electronic Resource
    Electronic Resource
    Stimulation of the synthesis of catecholamines in a sympathetic ganglion via cholinergic and non-cholinergic mechanisms (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 333 (1986), S. 17-22 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00569654
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  • 3
    Electronic Resource
    Electronic Resource
    Increase in brain dopamine after axotomy or treatment with gammahydroxybutyric acid due to elimination of the nerve impulse flow (1973)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 278 (1973), S. 347-361 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00501479
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  • 4
    Electronic Resource
    Electronic Resource
    R 28935 and prazosin: Effects on central and peripheral alpha-adrenoreceptor activity and on blood pressure (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 302 (1978), S. 299-306 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline ; Dopamine ; Alpha-adrenoreceptors ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effects of erythro-1-{1-[2-(1,4-benzodioxan-2-yl)-2-hydroxyethyl]-4-piperidyl}-2-benzimidazolinone (R 28935), prazosin and phenoxybenzamine on the clonidine-induced increases in the flexor relfex activity and in the blood pressure of rats were used to study their influence on postsynaptic α-adreno-receptors centrally and peripherally, respectively. R 28935 was more potent in blocking the central than the peripheral α-adrenoreceptors whereas the two receptor types were inhibited to about the same degree following prazosin and phenoxybenzamine. 2. The amphetamine-induced rotation of rats with unilateral inactivation of the corpus striatum and the apomorphine-induced stimulation of the motor activity of mice were inhibited by R 28935, but not by prazosin, indicating that R 28935 can block postsynaptic dopaminergic receptors. 3. The α-methyltyrosine-induced disappearance of noradrenaline in the brain and the spinal cord of rats was only slightly accelerated by prazosin but was more effectively accelerated by R 28935 and phenoxybenzamine. The deceleration by clonidine of the α-methyltyrosine-induced disappearance of noradrenaline was partially inhibited by R 28935 but was not influenced by prazosin indicating that central α-autoreceptors (presynaptic α-receptors) are only weakly blocked by R 28935 and not at all blocked by prazosin. 4. The blood pressure of intact rats was lowered by prazosin and phenoxybenzamine at doses effectively blocking vascular α-adrenoreceptors. On the other hand, R 28935 caused hypotension at doses blocking central but not peripheral α-adrenoreceptors suggesting that the hypotension might be due to inhibition of central noradrenergic neurotransmission.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508299
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  • 5
    Electronic Resource
    Electronic Resource
    Selective stimulation of dopamine and noradrenaline autoreceptors by B-HT 920 and B-HT 933, respectively (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 321 (1982), S. 100-104 
    Details
    ISSN: 1432-1912
    Keywords: Dopamine ; Noradrenaline ; Autoreceptors ; Postsynaptic receptors ; Sedation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The azepine derivatives B-HT 920 and B-HT 933 did not increase the motor activity of mice pretreated with reserpine or reserpine plus apomorphine, indicating that they do not stimulate postsynaptic dopamine receptors or noradrenaline α1-receptors in the brain. 2. The motor activity of mice not pretreated with reserpine was reduced by a low dose of B-HT 920 and by B-HT 933. The α1-adrenoceptor antagonist yohimbine reversed the sedation induced by B-HT 933, but not that induced by B-HT 920. 3. B-HT 933 and a high dose of B-HT 920 retarded the α-methyltyrosine-induced disappearance of noradrenaline in the mouse brain by a yohimbine-sensitive mechanism. 4. The α-methyltyrosine-induced disappearance of dopamine in the mouse brain was decelerated by a low dose of B-HT 920 and to a smaller degree by B-HT 933. The effects were inhibited by the dopamine receptor antagonist haloperidol. The effect of B-HT 933, but not that of B-HT 920, was partly antagonized by yohimbine. 5. The enhanced synthesis of dopamine in the corpus striatum of mice following treatment with gammabutyrolactone was completely antagonized by B-HT 920, but not by B-HT 933, via a haloperidol-sensitive mechanism. The synthesis of noradrenaline in the brain stem and in the hemispheres was reduced by B-HT 933 via a yohimbine-sensitive mechanism. 6. The results indicate that B-HT 920 can selectively and potently stimulate dopamine autoreceptor and that B-HT 933 can preferentially stimulate noradrenaline autoreceptors (α2-adrenoreceptors). These actions might cause the decreases in motor activity observed in mice not pretreated with reserpine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00518475
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of locally applied dopamine to the nucleus accumbens on the motor activity of normal rats and following α-methyltyrosine or Reserpine (1979)
    Springer
    Psychopharmacology 63 (1979), S. 203-206 
    Details
    ISSN: 1432-2072
    Keywords: Dopamine ; Nucleus accumbens ; Autoreceptors ; Release by nerve impulses
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The motor activity of rats was investigated following bilateral application of various doses (0–80 μg) of dopamine to the nucleus accumbens. A high dose (80 μg) of dopamine increased the motor activity of normal as well as α-methyltyrosine- and reserpine-treated rats. It also increased the late motor activity (6–9 min) of normal rats, probably due to stimulation of postsynaptic dopamine receptors. Lower doses (10–40 μg) of dopamine suppressed initial (0–3 min) motor activity of normal rats, perhaps due to stimulation of dopamine autoreceptors on the dopamine nerve terminals in the nucleus accumbens with a subsequent inhibition of dopamine neurotransmission. An intermediate dose (40 μg) of dopamine was able to restore the motor activity of α-methyltyrosine-treated but not of reserpine-treated rats at all time intervals. This difference, indicating a restoration of the normal pattern of habituation by dopamine only in animals pretreated with α-methyltyrosine, suggests that normal behaviour is dependent on release of dopamine by nerve impulses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00433550
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  • 7
    Electronic Resource
    Electronic Resource
    A functional effect of dopamine in the nucleus accumbens and in some other dopamine-rich parts of the rat brain (1975)
    Springer
    Psychopharmacology 45 (1975), S. 139-149 
    Details
    ISSN: 1432-2072
    Keywords: Locomotor activity ; Nucleus accumbens ; Caudate nucleus ; Local application ; Dopamine ; Noradrenaline ; Amphetamine ; Neuroleptics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Dopamine (5 to 50 Μg) applied bilaterally to the nucleus accumbens of reserpine-nialamide pretreated rats produced a marked dose-dependent rise in coordinated locomotor activity, devoid of stereotypies such as gnawing, rearing and licking seen after dopamine application (50 Μg) to the neostriatum. The locomotor activity was completely blocked by pimozide, but not by phenoxybenzamine. The effects of apomorphine or d-noradrenaline were similar to those of dopamine. In contrast, l-noradrenaline produced a “convulsive” syndrome devoid of coordinated locomotor activity, and this convulsive syndrome could be completely blocked by phenoxybenzamine but not by pimozide. Release of endogenous dopamine by d- or l-amphetamine (10 and 50 Μg) in the nucleus accumbens produced a rise in coordinated activity, the d-isomer was about 4 times as potent as the l-isomer, and the effect of the d-isomer was blocked completely by α-methyltyrosine. Bilateral application of trifluoperazine (2.5 Μg) to the nucleus accumbens completely blocked the effect of systemically administered d-amphetamine (1.5 and 3.0 mg/kg), but similar application to the area of the central nucleus of the amygdala or the neostriatum was much less effective. Partial protection of the endogenous dopamine stores against the depleting action of reserpine by local application of metatyramine to the nucleus accumbens resulted in a higher level of basal activity than in control animals. Application of dopamine or noradrenaline to the area of the central nucleus of the amygdala or to the olfactory tubercles did not lead to any consistent changes in locomotor activity. The nucleus accumbens and olfactory tubercles contained most of the dopamine in the limbic forebrain, with noradrenaline more evenly distributed. These data suggest that the nucleus accumbens plays an important role in the locomotor activity in rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00429052
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  • 8
    Electronic Resource
    Electronic Resource
    Inhibitory effect of gammahydroxybutyric acid and gammaaminobutyric acid on the dopamine cells in the substantia nigra (1973)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 279 (1973), S. 89-92 
    Details
    ISSN: 1432-1912
    Keywords: Gammahydroxybutyric Acid ; GABA ; Substantia nigra ; Inhibition ; Dopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Injections of gammahydroxybutyric acid or gammaaminobutyric acid (GABA), but not betahydroxybutyric acid or carnitine, into the substantia nigra induced increases in brain dopamine of rats. No effect was found after injections into the neostriatum. The noradrenaline in the forebrain was unchanged after all the treatments. Gammahydroxybutyric acid may act by directly or indirectly mimicking an inhibitory GABA mechanism on the dopamine cells in the substantia nigra.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00502071
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  • 9
    Electronic Resource
    Electronic Resource
    Effect of anaesthetic agents on the synthesis and disappearance of brain dopamine normally and after haloperidol, KCl or axotomy (1974)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 283 (1974), S. 409-418 
    Details
    ISSN: 1432-1912
    Keywords: Dopamine ; Pentobarbital ; Halothane ; Haloperidol ; Depolarization ; Axotomy ; Turnover ; Feedback
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The synthesis of dopamine was determined as the accumulation of Dopa after Dopa decarboxylase inhibition. The release of dopamine was determined as the disappearance of the amine after treatment with the tyrosine hydroxylase inhibitor α-methyltyrosine. These processes were not significantly changed in the rat brain by pentobarbital sodium anaesthesia or by 10 min halothane anaesthesia. The accelerations of the dopamine synthesis and release after treatment with haloperidol were markedly reduced during pentobarbital, but not halothane anaesthesia. Anaesthesia with pentobarbital did not affect the increased synthesis and release of dopamine observed when the dopaminergic nerve terminals were depolarized by local treatment with KCl. The increases in dopamine synthesis and concentration after axotomy were similar whether the operation was performed during pentobarbital or halothane anaesthesia. It is suggested that the selective reduction of the haloperidol-induced effects by pentobarbital may be due to interference with a neuronal feedback loop.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501113
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  • 10
    Electronic Resource
    Electronic Resource
    FLA 136: Selective agonist at central alpha-adrenoreceptors mediating changes in the turnover of noradrenaline (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 298 (1977), S. 239-243 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline ; Dopamine ; Utilization ; Synthesis ; Central alpha-adrenoreceptors ; Presynaptic receptors ; Postsynaptic receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. FLA 136 [4-amino-3-(2,6-dichlorobenzylidenehydrazino)-1,2,4-triazol] did not change the hindlimb flexor reflex of spinal rats, but it reduced the clonidine-induced increase in this reflex at high doses. 2. The α-methyltyrosine-induced disappearance of noradrenaline in the rat central nervous system was decelerated by FLA 136, with a peak effect after 15 mg/kg i.p. The accumulation of Dopa following decarboxylase inhibition was inhibited by FLA 136 (15 mg/kg i.p.) in a noradrenaline-predominant region (brain stem). The effect on the utilization appeared to be greater than that on the synthesis in agreement with a slight increase observed in the concentration of noradrenaline in the brain and the spinal cord. 3. FLA 136 reduced the α-methyltyrosine-induced disappearance of dopamine, decreased the Dopa accumulation following decarboxylase inhibition in the dopamine-rich corpus striatum and increased the concentration of dopamine. These effects might be secondary to inhibition of the noradrenergic neurotransmission. 4. Yohimbine almost completely inhibited the effect of FLA 136 on the utilization and on the synthesis of noradrenaline whereas phenoxybenzamine was much less effective on the change in the utilization. Yohimbine and phenoxybenzamine were about equipotent, however, in accelerating the disappearance of noradrenaline produced by α-methyltyrosine alone. 5. FLA 136 does not stimulate the postsynaptic α-adrenoreceptors mediating the increase in flexor reflex activity but it probably decelerates the utilization of noradrenaline by a stimulation of another kind of α-adrenoreceptors sensitive to yohimbine. The latter receptors might occur on the noradrenergic neurones (presynaptic receptors).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500894
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