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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 137 (1994), S. 119-125 
    ISSN: 1432-1424
    Keywords: Neuroblastoma cells ; K+ channels ; Vacuolar H+-ATPase ; Resting potential
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract The aim of this work was to examine the effects of changes in external K+ concentration (K o ) around its physiological value, of various K+ channels blockers, including internal Cs+, of vacuolar H+-ATPase inhibitors and of the protonophore CCCP on the resting potential and the voltage-dependent K+ current of differentiated neuroblastoma x glioma hybrid NG108-15 cells using the whole-cell patch-clamp technique. The results are as follows: (i) under standard conditions (K o =5 mm) the membrane potential was −60±1 mV. It was unchanged when K o was decreased to 1 mm and was depolarized by 4±1 mV when Ko was increased to 10 mm. (ii) Internal Cs+ depolarized the membrane by 21±3 mV. (iii) The internal application of the vacuolar H+-ATPase inhibitors N-ethylmaleimide (NEM), NO 3 − and bafilomycin A1 (BFA) depolarized the membrane by 15±2, 18±2 and 16±2 mV, respectively, (iv) When NEM or BFA were added to the internal medium containing Cs+, the membrane was depolarized by 45±1 and 42±2 mV, respectively. (v) The external application of CCCP induced a transient depolarization followed by a prolonged hyperpolarization. This hyperpolarization was absent in BFA-treated cells. The voltage-dependent K+ current was increased at negative voltages and decreased at positive voltages by NEM, BFA and CCCP. Taken together, these results suggest that under physiological conditions, the resting potential of NG108-15 neuroblastoma cells is maintained at negative values by both voltage-dependent K+ channels and an electrogenic vacuolar type H+-ATPase.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 244 (1996), S. 2-8 
    ISSN: 1432-1459
    Keywords: Key words Parkinson’s disease ; Cognitive deficits ; Executive ; functions ; Dementia ; Dopaminergic systems
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Neuropsychological investigations of patients with Parkinson’s disease have shown specific impairments even in the early stages of the disease, which include deficit of behavioural regulation in sorting or planning tasks, defective use of memory stores, and impaired manipulation of internal representation of visuospatial stimuli. These deficits, reported in a disease which predominantly involves subcortical structures, have drawn attention to a potential role of the basal ganglia in cognitive processes. Given the modulatory role of the basal ganglia, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategies, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity or complementarity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of segregated loops that interconnect discrete regions of the caudate nucleus to the dorsolateral and orbitofrontal regions of the prefrontal cortex via the thalamus may give some support to this hypothesis. Alternatively, degeneration of the ascending cholinergic and catechola- minergic neuronal systems may contribute, at least in part, to the occurrence of this frontal-lobe-like symptomatology associated with Parkinson’s disease.
    Type of Medium: Electronic Resource
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