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  • 1980-1984  (2)
  • 1980  (2)
  • Cerebral cortex  (2)
  • Ca2+ antagonists  (1)
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Years
  • 1980-1984  (2)
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Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 40 (1980), S. 247-250 
    ISSN: 1432-1106
    Keywords: Extracellular Ca2+ activity ; Cerebral cortex ; Excitatory aminoacids ; Ca2+ antagonists ; GABA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Extracellular Ca2+ activity (aCa) changes were measured with Ca2+-sensitive microelectrodes in the cat cerebral cortex during iontophoretic administration of excitatory and inhibitory aminoacids. Glutamate, aspartate and DL homcysteate usually decreased aCa from a baseline of 1.3 mM to as low as 0.1 mM. The amplitude of the changes was largest at depths between 100 and 300 μm beneath the cortical surface. The aCa decreases could be deminished or blocked by Co2+, Mn2+ or La3+ as well as by GABA. These data suggest that large Ca2+ conductances that may be voltage-sensitive are present in apical dendrites of neocortical neurones.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    ISSN: 1432-1106
    Keywords: Extracellular space ; K+ regulation ; Spatial K+ buffering ; Epilepsy ; Cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The time course of local changes of the extracellular space (ES) was investigated by measuring concentration changes of repeatedly injected tetramethylammonium (TMA+) and choline (Ch+) ions for which cell membranes are largely impermeable. After stimulus-induced extracellular [K+] elevations the δ[TMA+] and δ[Ch+] signals recorded with nominally K+-selective liquid ion-exchanger microelectrodes increased by up to 100%, thus indicating a reduction of the ES down to one half of its initial size. The shrinkage was maximal at sites where the K+ release into the ES was also largest. At very superficial and deep layers, however, considerable increases in extracellular K+ concentration were not accompanied by significant reductions in the ES. These findings can be explained as a consequence of K+ movement through spatially extended cell structures. Calculations based on a model combining the spatial buffer mechanism of Kuffler and Nicholls (1966) to osmolarity changes caused by selective K+ transport through primarily K+ permeable membranes support this concept. Following stimulation additional iontophoretically induced [K+]o rises were reduced in amplitude by up to 35%, even at sites where maximal decreases of the ES were observed. This emphasizes the importance of active uptake for K+ clearance out of the ES.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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