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  • Cerebellum  (2)
  • Diazepam  (2)
  • Septum  (2)
  • Chemistry
  • Springer  (5)
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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 296 (1977), S. 117-121 
    ISSN: 1432-1912
    Keywords: Cerebellum ; cGMP ; Morphine ; Mossy fibers ; Climbing fibers ; Striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Morphine, dextromoramide (4 μmol/kg i.p.) and vimonol R2 (17 μmol/kg i.p.) in analgesic doses (28 to 112 μmol/kg i.p.) decreased 3′,5′-cyclic guanosine monophosphate (cGMP) in rat cerebellar cortex; morphine also decreased the cGMP content in deep cerebellar nuclei. Intrastriatal but not intracerebellar injections of morphine (20 μg) decreased cerebellar cGMP content. Naltrexone, an opiate receptor antagonist, but not apomorphine, a dopaminergic receptor agonist, blocked the effect of morphine on cerebellar cGMP. Pretreatment with 3-acetylpyridine (3-AP) which destroys the climbing fibers, failed to antagonize the effect of morphine on cerebellar cGMP. These results suggest that activation of opiate receptors in striatum decreases cerebellar cGMP content presumably by reducing activity in the mossy fiber excitatory input to cerebellum.
    Type of Medium: Electronic Resource
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  • 2
    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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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 289 (1975), S. 369-378 
    ISSN: 1432-1912
    Keywords: cGMP ; Isoniazid ; Cerebellum ; GABA ; Picrotoxin ; Diazepam ; Convulsions
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Subcutaneous injections of isoniazid or picrotoxin increase the cerebellar content of 3′,5′-cyclic guanosine monophosphate (cGMP) without changing the 3′,5′-cyclic adenosine monophosphate cAMP. This increase was dose dependent and the threshold for the cGMP increase was lower than that for convulsions. In cerebellum the increase of cGMP content elicited by isoniazid but not that caused by picrotoxin was paralleled by a decrease of GABA content. Diazepam doses starting from 1.74 μmol/kg intraperitoneally produced a dose dependent decrease of cerebellar cGMP concentration without changing cAMP or GABA content. Smaller doses of diazepam (0.5 μmol/kg i.p.) failed to decrease the basal cerebellar content of cGMP. However, this dose of diazepam antagonized the increase of cGMP produced by isoniazid but not that produced by picrotoxin. Higher doses of diazepam were necessary to block the increase of cerebellar cGMP elicited by picrotoxin. Low doses of diazepam (0.14 μmol/kg) antagonized the convulsions in 50% of the rats injected with 3.3 mmol/kg of isoniazid. The doses of diazepam required to block picrotoxin, pentylenetetrazol or strychnine convulsions were 7, 25 and 40 times higher than those required to block isoniazid convulsions, respectively. Desmethyldiazepam, chloridiazepoxide, oxazepam were also several times more potent in antagonizing isoniazid than picrotoxin, pentylenetetrazol, or strychnine convulsions. In contrast, barbiturates were equipotent against all the convulsants studied. These experiments suggest that diazepam may act in the CNS either by altering the disposition of endogenous GABA or by mimicking the action of GABA at specific synaptic receptors.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 294 (1976), S. 251-255 
    ISSN: 1432-1912
    Keywords: Diazepam ; Muscimol ; Acetylcholine turnover ; GABA receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Muscimol (8.8 μmol/kg i.v.) and diazepam (7.04 μmol/kg i.p.) decreased the rate of turnover of acetylcholine in midbrain and cortex of rat brain but failed to change acetylcholine turnover in striatum and hippocampus. The similarity in the profile of the action of diazepam and muscimol on acetylcholine turnover in various brain structures adds support to the view thet GABA participates in mediating the actions of diazepam. Since the striatum contains an abundance of GABA neurones and intrinsic cholinergic neurones, it is inferred that the metabolism of acetylcholine, and presumably the activity of striatal cholinergic neurones are not regulated by the activation of GABA receptors. Similar considerations apply to the cholinergic pathway projecting from the septum to the hippocampus.
    Type of Medium: Electronic Resource
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  • 5
    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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