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  • 1
    Electronic Resource
    Electronic Resource
    Effects of penfluridol on dopamine-sensitive adenylate cyclase in corpus striatum and substantia nigra of rats (1976)
    Springer
    Cellular and molecular life sciences 32 (1976), S. 1558-1559 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Penfluridol, a neuroleptic with diphenylbutyl piperidine structure, blocked the dopamine-sensitive adenylate cyclase in homogenates of corpus striatum and substantia nigra of rats, probably by a competitive antagonism versus dopamine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01924451
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  • 2
    Electronic Resource
    Electronic Resource
    Dopamine-sensitive adenylate cyclase in homogenates of rat striata during ethanol and barbiturate withdrawal (1976)
    Springer
    Archives of toxicology 35 (1976), S. 247-253 
    Details
    ISSN: 1432-0738
    Keywords: Dopamine receptors ; Adenyl cyclase ; Corpus striatum ; Ethanol withdrawal ; Barbiturate withdrawal ; Dopamin-Rezeptoren ; Adenyl-Cyclase ; Corpus striatum ; Äthanolentzug ; Barbituratentzug
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Nach wiederholter Gabe von Äthanol oder von Phenobarbital an Ratten wurden die Substanzen abgesetzt und dadurch charakteristische Entzugssymptome hervorgerufen. Weil beide Substanzen den Dopaminstoffwechsel im Gehirn beeinflussen, wurde die postsynaptische Empfindlichkeit gegenüber Dopamin in den Corpora striata während des Äthanol- bzw. Phenobarbital-Entzuges geprüft. Dies erfolgte, indem die Dopamin-empfindliche Adenylat-Cyclase in Homogenaten der Corpora striata untersucht wurde. Die Resultate zeigten eine leicht herabgesetzte Empfindlichkeit gegenüber Dopamin im Entzug von Äthanol oder Phenobarbital. Beide Substanzen beeinflußten, wenn sie in vitro den Homogenaten zugesetzt wurden, nicht die postsynaptische Empfindlichkeit gegenüber Dopamin. Im Falle des Dopamins konnte also nicht die Hypothese unterstützt werden, daß eine erhöhte postsynaptische Empfindlichkeit gegenüber den zugehörigen Neurotransmittern für Entzugs-Symptome nach chronischer Verabreichung von Substanzen, die körperliche Abhängigkeit hervorrufen, von Bedeutung ist.
    Notes: Summary Repeated administrations of ethanol and of phenobarbital to rats led to characteristic withdrawal symptoms when the drug had been stopped. Since both drugs affect brain dopamine metabolism, the postjunctional sensitivity to dopamine in the corpora striata was tested during ethanol or phenobarbital withdrawal. This was done by studying the dopamine-sensitive adenylate cyclase in homogenates of the corpora striata of ethanol- or phenobarbital-dependent rats. The results demonstrated a slight postjunctional subsensitivity to dopamine in withdrawal from both ethanol and phenobarbital. Both drugs, when added in vitro, did not affect the postjunctional sensitivity to dopamine. The results do not support the hypothesis, at least not in the case of dopamine, that a postjunctional supersensitivity to neurotransmitters is important for withdrawal symptoms after chronic administration of drugs inducing physical dependence.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00570266
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  • 3
    Electronic Resource
    Electronic Resource
    Inhibition by opiate narcotics of rat flexor α-motoneurones (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 301 (1978), S. 181-185 
    Details
    ISSN: 1432-1912
    Keywords: Motoneurones ; Flexor α-motoneurones ; Opiate narcotics ; Morphine ; Naloxone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Specific effects of opiate narcotics on rat flexor α-motoneurones were studied in ventral roots of laminectomized rats under halothane anaesthesia. The α-motoneurones were activated by tetanic stimulation of the cut ipsilateral common peroneal nerve, exciting up to group II- but not group III- and C-afferents. Morphine (0.5–3.0 mg/kg i.v.) reduced or completely suppressed the discharge rate of flexor α-motoneurones in a dose-dependent manner. This effect was antagonized by naloxone (0.5 mg/kg i.v.) and mimicked by levorphanol (1.0 mg/kg i.v.), but not by an equal dose of its steroisomer dextrorphan, suggesting that the effect described is a specific one. After spinalization, the inhibitory effect of morphine was abolished. Previous studies had shown that opiates (e.g. morphine, given in a dose of 2 or 4 mg/kg i.v.) excite rat extensor α-motoneurones, an effect opposite to the opiate narcotic action on flexor α-motoneurones. The action of opiates leading to an inhibition of flexor α-motoneurones may contribute to akinesia and catalepsy, and opioid-induced muscular rigidity. From the results presented it appears that morphine produces a reciprocal change in the activity evoked in extensor and flexor reflex pathways.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00507035
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of haloperidol on reflex activation of rat α-motoneurones (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 308 (1979), S. 149-154 
    Details
    ISSN: 1432-1912
    Keywords: α-Motoneurones ; Haloperidol ; Apomorphine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of haloperidol on rat flexor and extensor α-motoneurones were studied in ventral roots of laminectomized rats under halothane anesthesia. The α-motoneurones were activated by tetanic stimulation of low-threshold afferents (group I and II), either of the ipsilateral peroneal nerve (“flexor α-motoneurones”) or gastrocnemius-soleus nerve (“extensor α-motoneurones”). Haloperidol, given in the doses of 0.075, 0.15 and 0.30 mg/kg i.p. inhibited the reflex activation of flexor α-motoneurones; higher doses seemed to be more effective than lower ones. Apomorphine (2 mg/kg s.c.) partially antagonized the inhibitory action of haloperidol with some latency. Higher doses of haloperidol (0.15–0.60 mg/kg i.p.) also inhibited the reflex activation of extensor α-motoneurones; this inhibitory effect was, at least for a short time, antagonized by apomorphine (2 mg/kg s.c.). The threshold for reflex activation both of flexor and extensor α-motoneurones was raised by haloperidol and lowered by a subsequent administration of apomorphine. Our results suggest that akinesia and catalepsy, induced in rats by haloperidol might be, at least in part, due to a decrease in sensitivity of α-motoneurones to proprioceptive stimuli.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499057
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    Paper (German National Licenses)
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