1,720,966 research outputs found
5-hydroxytryptamine3 receptors sited on cholinergic axon terminals of human cerebral cortex mediate inhibition of acetylcholine release
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Pirenzepine-insensitive muscarinic autoreceptors regulate acetylcholine release in human neocortex
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Enhancement of glycine release from human brain cortex by acetylcholine acting at M4 muscarinic receptors
No full textRelease-regulating autoreceptors of the GABAB-type in human cerebral cortex
No full text1. The depolarization-evoked release of gamma-aminobutyric acid (GABA) and its modulation mediated by autoreceptors were investigated in superfused synaptosomes prepared from fresh human cerebral cortex. 2. The release of [3H]-GABA provoked by 15 mM K+ from human cortex nerve endings was almost totally (85%) calcium-dependent. 3. In the presence of the GABA uptake inhibitor SK&F 89976A (N-(4,4-diphenyl-3-butenyl)-nipecotic acid), added to prevent carrier-mediated homoexchange, GABA (1-10 microM) decreased in a concentration-dependent manner the K+-evoked release of [3H]-GABA. The effect of GABA was mimicked by the GABAB receptor agonist (-)-baclofen (1-100 microM) but not by the GABAA receptor agonist muscimol (1-100 microM). Moreover, the GABA-induced inhibition of [3H]-GABA release was not affected by two GABAA receptor antagonists, bicuculline or SR 95531 (2-(3'-carbethoxy-2'-propenyl)-3-amino-6-paramethoxy-phenyl-pyr idazinium bromide). 4. (-)-Baclofen also inhibited the depolarization-evoked release of endogenous GABA from human cortical synaptosomes. 5. It is concluded that GABA autoreceptors regulating the release of both newly taken up and endogenous GABA are present in human brain and appear to belong to the GABAB subtype
Choroid plexus carcinoma. Case report
No full textPlexus-chorioideus carcinomata or malignant plexus papillomas are very rare; only few cases have been described in the literature. A further observation is added now. In a 13-year-old girl, signs of brain pressure occured two weeks before admission to a hospital. Scintigraphy and vertebral angiography showed a process in the atrium of the right lateral ventricle which was removed by temporo-parietal trephination. The tumour had the size of an apricot and a reddish colouration, it proceeded from the plexus. After-irradiation with 5 000 rad. Six years after the operation, signs of brain pressure appeared again. Neuroradiologically the process was located in the right cerebellar hemisphere. After trephination of the cerebellum, the largely vascularised tumour, which appeared to originate from the tela choroidea of the 4th ventricle, could be removed. The further course was without pathological findings. Histologically, the typical criteria were found: Invasion of surrounding brain structures, loss of the regular papillary structure, malignisation of the cells and originating from the plexus choroideus
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