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  • 1
    Electronic Resource
    Electronic Resource
    ACCUMULATION AND DISAPPEARANCE OF NORADRENALINE AND ITS MAJOR METABOLITES SYNTHESIZED FROM INTRAVENTRICULARLY INJECTED [3H]DOPAMINE IN THE RAT BRAIN (1974)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 23 (1974), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— A new combined ion-exchange and thin-layer-chromatographic procedure is described which separates and measures quantitatively, after intraventricular injection of [3H]dopamine (DA), the rat brain content of labelled noradrenaline (NA) and the following labelled noradrenaline metabolites: free 3-methoxy-4-hydroxyphenylethyleneglycol (MOPEG), conjugated MOPEG, free plus conjugated dihydroxyphenylethyleneglycol (DOPEG), vanillic mandelic acid (VMA) and normetanephrine (NM). Labelled dopamine and its metabolites were also measured. The time-course study performed from 5 min to 24 h after [3H]DA showed that MOPEG and DOPEG, mainly as conjugates, are major NA metabolites whereas VMA is a very insignificant NA metabolite in the rat brain. A very rapid initial increase of [3H]NM, free MOPEG and conjugated MOPEG was found during the time interval where the [3H]NA biosynthesis is very high (0–15 min). This combined with the finding that these metabolites stabilize at lower levels during the [3H]NA ‘storage phase’ (9–24 h) provides a strong indication that newly synthesized NA preferentially is metabolized. Our measurements of endogenous NA, free MOPEG and conjugated MOPEG provide additional support. The injections of various decreasing doses of [3H]DA (3·08–0·0010 μg) showed that the proportions of total [3H]MOPEG and total [3H]DOPEG to [3H]NA were constant after all [3H]DA doses investigated. This finding indicates that the [3H]NA synthesized in situ behaves as a tracer, even after injections of non-tracer doses of [3H]DA. The results seem thus to indicate that the present technique provides a powerful tool for the investigations on central noradrenaline metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1974.tb06061.x
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  • 2
    Electronic Resource
    Electronic Resource
    Protriptyline induced inhibition of the in vivo 3H-noradrenaline synthesis from 3H-l-Dopa in the rat brain (1974)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 285 (1974), S. 15-28 
    Details
    ISSN: 1432-1912
    Keywords: Protriptyline ; Noradrenaline Biosynthesis ; 3H-l-Dopa ; 3H-l-Tyrosine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 3H-l-Dopa was given intraperitoneally, after a peripheral decarboxylase inhibitor Ro 4-4602 (50 mg/kg), to male Wistar rats and the effect of protriptyline pretreatment (10 mg/kg, 30 min) on the formation and metabolism of the brain 3H-catecholamines, dopamine and noradrenaline and all their metabolites was investigated. Protriptyline produced a strong decrease of labelled noradrenaline and its metabolites normetanephrine, free and conjugated 3-methoxy-4-hydroxyphenyl-eneglycol and 3,4-dihydroxyphenyleneglycol 60 and 120 min after 3H-l-Dopa. 3H-noradrenaline was also decreased 30 and 45 min after 3H-l-Dopa. In rats and mice the pretreatment with protriptyline (10 mg/kg, 30 min) induced also a significant decrease in brain 3H-noradrenaline but not 3H-dopamine synthesized from 3H-l-tyrosine. Protriptyline (10 mg/kg) produced no effect on endogenous dopamine and noradrenaline in the rat or mouse brain. The present findings strongly indicate that the acute treatment with protriptyline inhibits the 3H-noradrenaline formation from 3H-l-Dopa. This effect seems most likely to be related to an interaction of protriptyline with the precursor(s) 3H-l-Dopa or 3H-dopamine at sites of 3H-noradrenaline biosynthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499525
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  • 3
    Electronic Resource
    Electronic Resource
    Behavioral differences induced by muscimol selectively injected into pars compacta and pars reticulata of Substantia Nigra (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 310 (1979), S. 43-51 
    Details
    ISSN: 1432-1912
    Keywords: GABA receptors ; Dopamine receptors ; Turning behavior ; Substantia Nigra ; Nigro-striatal system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Turning behavior was recorded after injection of the GABA agonist muscimol into the caudal part of rat substantia nigra, pars compacta (SNC) or pars reticulata (SNR). Unilateral injection of muscimol (10–25 ng) into SNC induced ipsilateral body posture. Additional treatment with apomorphine (0.5 mg/kg, s.c.) produced intense ipsilateral turning. This effect was abolished in rats depleted of catecholamines by the combined treatment with reserpine plus α-methyltyrosine. The ipsilateral turning was probably not mediated via inhibition of dopaminergic (DA) activity since unilateral SNC injections of the DA agonist apomorphine (2.5–10 μg) in contrast produced contralateral turning upon systemic apomorphine administration. Unilateral injection of muscimol into SNR induced strong contralateral turning, resistant to DA receptor blockade. In contrast, the contralateral turning was dose dependently antagonized by apomorphine (0.1–5 mg/kg, s.c.). Locally applied apomorphine (2.5–20 μg) into SNR, striatum or nucleus accumbens also antagonized intranigral muscimol, corpus striatum being the most sensitive area. Bilateral intrastriatal apomorphine was most effective, followed by unilateral injection into the ipsilateral striatum. The apomorphine antagonism was attenuated by additional haloperidol treatment, possibly indicating DA-specificity. Systemic amphetamine (2 mg/kg, i.p.) or local injection of the DA agonist ADTN (10–20 μg) into SNR, striatum or nucleus accumbens was without inhibitory effect on intranigral muscimol. These results suggest that the interaction between DA and nigral GABA is extremely complex: 1. Differential functional effects of a GABA agonist are found within SNC and SNR; 2. The turning behavior induced by muscimol injected into SNR is antagonized by stimulation of apomorphine sensitive DA receptors but not by those activated by amphetamine or ADTN, and 3. The inhibitory effect of apomorphine is observed following injection into several DA containing structures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499873
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  • 4
    Electronic Resource
    Electronic Resource
    The effect of amitriptyline, desipramine and imipramine on the in vivo brain synthesis of 3H-noradrenaline from 3H-l-dopa in the rat (1975)
    Springer
    Psychopharmacology 41 (1975), S. 249-254 
    Details
    ISSN: 1432-2072
    Keywords: Amitriptyline ; Desipramine ; Imipramine ; Noradrenaline Biosynthesis ; 3H-l-Dopa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 3H-l-Dopa was given to rats after a peripheral decarboxylase inhibitor Ro 4-4602 (50 mg/kg) and the effect of 30 min pretreatment with amitriptyline (10 mg/kg), desipramine (10 mg/kg) and imipramine (10 mg/kg) on the brain formation of 3H-dopamine, 3H-noradrenaline and their major metabolites was investigated. Desipramine produced a decrease in the level of labelled noradrenaline and its major metabolites free and conjugated 3-methoxy-4-hydroxyphenyleneglycol and 3,4-dihydroxyphenyleneglycol. Imipramine decreased labelled noradrenaline and 3-methoxy-4-hydroxyphenyleneglycol, whereas amitriptyline produced no significant effect on noradrenaline metabolism. The thymoleptic drugs produced no significant effect on endogenous brain noradrenaline and dopamine. These findings provide a strong indication that desipramine and imipramine inhibit the 3H-noradrenaline biosynthesis from 3H-l-Dopa. The effect seems closely related to the wellknown membrane inhibitory effect of these drugs, since desipramine produced a more marked effect than imipramine and amitriptyline showed no effect. No conclusive evidence for the precise mechanism of action was obtained but it is possible that the decreased 3H-noradrenaline synthesis is related to interference of desipramine and imipramine with the precursor(s) 3H-l-Dopa or 3H-dopamine at sites of 3H-noradrenaline biosynthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00428932
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  • 5
    Electronic Resource
    Electronic Resource
    Evidence for increased apomorphine-sensitive dopaminergic effects after acute treatment with morphine (1977)
    Springer
    Psychopharmacology 53 (1977), S. 55-63 
    Details
    ISSN: 1432-2072
    Keywords: Apomorphine ; Morphine ; Behavioral effects ; Dopaminergic mechanisms ; Serotonin ; Mice ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Apomorphine in a very small non-stimulant dose 0.05 mg/kg s.c. antagonized the locomotor stimulant effect of morphine (50 mg/kg) in mice. Apomorphine (0.05 mg/kg) antagonized also the locomotor stimulant effect of a single low dose of morphine (2 mg/kg) in the rat as well as “the late stimulatory effect” seen after a higher dose of morphine (10 or 20 mg/kg). The pretreatment with morphine in increasing doses induced an increasing degree of potentiation of stereotyped behavior induced by high doses of apomorphine (0.5 and 2 mg/kg s.c.) in the rat. The apomorphine stereotyped biting/gnawing activity was found strongly increased by morphine (10–50 mg/kg) during the time interval where morphine given alone induced catalepsy. Our results indicate that the acute treatment with morphine may induce an increase of apomorphine sensitive dopaminergic mechanisms. The inhibitory effect by a very small dose of apomorphine (0.05 mg/kg) of morphine stimulation may be due to a presynaptic dopamine receptor stimulant effect of apomorphine. The antagonism by the serotonin antagonist methergoline of morphine catalepsy and the increase by this drug of “the late morphine excitation” indicate in addition a role of a serotonergic mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00426694
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