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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 103 (1996), S. 651-660 
    ISSN: 1435-1463
    Keywords: Dizocilpine (MK-801) ; N-methyl-D-aspartate ; acetylcholine ; dopamine receptors ; in vivo microdialysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of dopaminergic receptor antagonists on dizocilpineinduced increase in extracellular acetylcholine (ACh) levels in the rat parietal cortex were examined in freely-moving rats, using an in vivo brain microdialysis method. Dizocilpine (0.5 mg/kg) significantly increased extracellular ACh levels in the rat parietal cortex and hippocampus, but not in the striatum. Pretreatment with α-methyl-p-tyrosine methyl ester (αMpT) delayed the onset but prolonged the duration of the dizocilpine-induced increases in extracellular ACh levels. The dopamine D2 receptor antagonist, haloperidol, showed dual effects similarly to αMpT, while the dopamine D1 receptor antagonist, SCH23390, prolonged, but did not delay, the onset of the dizocilpine-induced increases in ACh levels. These results suggest that the dopaminergic system is involved in the dizocilpine-induced increase in the extracellular ACh level in the parietal cortex in two ways, through both dopamine D1 and D2 receptors.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 94 (1988), S. 69-73 
    ISSN: 1432-2072
    Keywords: GABAergic neuronal system ; GABA antagonist ; GABA agonist ; Passive avoidance task ; Conditioned suppression task ; Memory ; Mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role of GABAergic neuronal system in learning and memory was investigated using the step-down typed passive avoidance and rapidly learned conditioned suppression tasks in mice. GABA antagonists, picrotoxin and bicuculline, or a GABA synthesis inhibitor, 3-mercaptopropionic acid (3-MP), were administered just after the training test. All of these drugs caused amnesia: they shortened the step-down latency (SDL) and attenuated the conditioned suppression of motility in the retention test conducted 24 h after the administration. Furthermore, we investigated the effect of GABA receptor agonists, muscimol and baclofen, or a GABA transaminase inhibitor, aminooxyacetic acid (AOAA), on these amnesia models. GABA agonists showed an antiamnesic action as follows: in the passive avoidance task, 1) picrotoxin-induced amnesia was antagonized by muscimol, baclofen and AOAA. 2) Bicuculline-induced amnesia was antagonized by muscimol and AOAA but not by baclofen. 3) 3-MP-induced amnesia was antagonized only by muscimol. 4) In the rapidly learned conditioned suppression task, picrotoxin-, bicuculline- and 3-MP-induced amnesia were antagonized by muscimol, baclofen and AOAA. These results suggest that the GABAergic neuronal system plays an important role in the memory retention of passive avoidance and rapidly learned conditioned suppression tasks.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-1463
    Keywords: MK-801 ; THC-induced catalepsy ; dopamine ; acetylcholine ; mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mice treated with Δ9-tetrahydrocannabinol (THC; 5 and 10mg/kg i.v.) showed the catalepsy in high bar test, and median descent latencies of catalepsy were about 150 sec. Dizocilpine (MK-801, 0.05 and 0.1mg/kg), non-competitive N-methyl-D-aspartate (NMDA) antagonist, significantly attenuated THC-induced catalepsy. Furthermore, the anticataleptic effect of MK-801 on THC-induced catalepsy was blocked by acetylcholine agonist oxotremorine (0.005 mg/kg) and dopamine antagonist haloperidol (0.01mg/kg), but not by NMDA. Oxotremorine, haloperidol, and NMDA themselves did not affect THC-induced catalepsy at the doses used. These results suggest that the anticataleptic effect of MK-801 on THC-induced catalepsy may be developed through dopaminergic and acetylcholinergic neuronal systems.
    Type of Medium: Electronic Resource
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