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  • Striatum  (3)
  • Cortex  (2)
  • 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
    ISSN: 1432-1912
    Keywords: Dopamine ; Haloperidol ; Adenylate cyclase ; Striatum ; Supersensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rats were injected daily with 1.3 μmol/kg of haloperidol s.c. for 10 days. From the second to the ninth day after haloperidol withdrawal the rats developed supersensitivity to the behavioral affects of apomorphine. Concomitantly, the K a of dopamine for the activation of striatal adenylate cyclase was lowered and the striatal content of the Ca2+ dependent protein that activates cAMP phosphodiesterase was increased. This activator protein is stored in striatal membranes and can be released by membrane phosphorylation in cytosol. This protein increases the activity of the high K m phosphodiesterase (Uzunov et al., 1976) but when it is bound to striatal membranes it facilitates the activation of striatal adenylate cyclase by dopamine (Gnegy et al., 1976 b). The increase in protein activator content of striatal membranes caused by haloperidol could be a primary factor in causing supersensitivity to the biochemical and behavioral effects of dopamine receptor agonists.
    Type of Medium: Electronic Resource
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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 304 (1978), S. 107-110 
    ISSN: 1432-1912
    Keywords: Δ9-Tetrahydrocannabinol ; Cannabidiol ; Hippocampus ; Cortex ; Striatum ; Acetylcholine ; Turnover rate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of Δ9-tetrahydrocannabinol, (Δ9THC) the major psychoactive compound of marijuana, and cannabidiol (CBD), a non-psychoactive component, on the acetylcholine (ACh) concentration and the turnover rate of ACh (TRACh) have been studied in various regions of the rat brain. Neither Δ9THC doses from 0.2 to 10 mg/kg nor CBD (10 or 20 mg/kg) alter the ACh concentration in the brain areas examined 30 min, after the intravenous injection. However, Δ9-THC (doses from 0.2 to 10 mg/kg) causes a marked dose-related decrease in the TRACh in hippocampus whereas CBD is without effect in this brain region even when 20 mg/kg is given. Furthermore, high doses of Δ9-THC (5 mg/kg) and CBD (20 mg/kg) that produce a significant decrease in the TRACh of striatum fail to change the TRACh in parietal cortex. The low doses of Δ9-THC required to reduce hippocampal TRACh suggest that an action on these cholinergic mechanisms may play a role in the psychotomimetic activity of Δ9-THC.
    Type of Medium: Electronic Resource
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