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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 299 (1977), S. 149-153 
    ISSN: 1432-1912
    Keywords: Morphine ; β-Endorphin ; Naltrexone ; Acetylcholine turnover ; Septum ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intraseptal administration of morphine (70 nmol) or β-endorphin (0.7 nmol) reduced the rate of acetylcholine (ACh) turnover (TRACh) in rat hippocampus but not in striatum or cortex. These intraseptal injections failed to modify the ACh content and did not elicit analgesia. Naltrexone (15 μmol/kg, i.p.) completely antagonized the decrease of hippocampal TRACh elicited by the two opiate receptor agonists. Furthermore, intraseptal injections of naltrexone partially blocked the decrease in hippocampal TRACh induced by intraperitoneal administration of morphine (70 μmol/kg, i.p.). These data suggest that opiate agonists decrease hippocampal TRACh by regulating septal cholinergic neurons, and that this effect is not associated with analgesia.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 304 (1978), S. 263-269 
    ISSN: 1432-1912
    Keywords: Apomorphine ; Amphetamine ; Antidepressant ; Nomifensine ; Cortex ; Hippocampus ; Septum ; Acetylcholine turnover
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acetylcholine (ACh) content and turnover rate (TRACh) have been measured in various brain regions of rats receiving the antidepressant nomifensine. The action of nomifensine was compared to that of amphetamine, apomorphine and several tricyclic antidepressants (amitriptyline, chlorimipramine, desipramine and iprindole). Nomifensine (14, 28 and 71 μmol/kg, i.p.) and amphetamine (27 μmol/kg, i.p.) increase TRACh in the cortex, hippocampus and diencephalon, but fail to change ACh content. Since both drugs release catecholamines, we tested the dopamine (DA) receptor agonist apomorphine (2.4 and 4.8 μmol/kg, s.c.) and found that it fails to change the TRACh or the ACh content in the cortex or diencephalon, but that it decreases TRACh in the hippocampus. Since apomorphine in doses that cause stereotypy fails to increase TRACh in cortex and hippocampus, one can infer that the increase in cortical and hippocampal TRACh caused by nomifensine and amphetamine is unrelated to their ability to cause stereotypy. Phenoxybenzamine (15 nmole) injected intraseptally fails to change hippocampal TRACh but blocks the nomifensine- and amphetamine-induced increase of TRACh in cortex and hippocampus. This indicates that the nomifensine- and amphetamine-induced increase of TRACh in the cortex and perhaps in the hippocampus is due to noradrenergic activation of the cholinergic neurons. The increase of TRACh caused by nomifensine is probably not related to its action on depression since none of the tricyclic antidepressants tested affects ACh content or TRACh in the brain regions examined. The only exception is amitriptyline, which decreases ACh content in the cortex and striatum.
    Type of Medium: Electronic Resource
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