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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Pharmacology, Biochemistry and Behavior 49 (1994), S. 769-772 
    ISSN: 0091-3057
    Keywords: Acetylcholine ; Alzheimer's disease ; Nicotine ; Senescence-accelerated mice (SAM) ; Tobacco
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 399 (1983), S. 54-62 
    ISSN: 1432-2013
    Keywords: Pancreas ; Acinar cell ; Voltage clamp ; Current transients ; Acetylcholine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Isolated segments of mouse pancreas were placed in a perspex bath and superfused with physiological saline solution. Acinar units were voltage-clamped with the help of two intracellular microelectrodes. Voltage homogeneity was in some experiments checked with a third microelectrode inserted into the same unit. The currents associated with hyper- or depolarizing voltage jumps were recorded in the absence or presence of sustained stimulation with acetylcholine (ACh), caerulein or bombesin nonapeptide. ACh (2×10−7−10−8 M) evoked a dose-dependent inward current and an increase in the membrane conductance. The steady state ACh-evoked current (control current subtracted from total current in presence of ACh) depended linearly on voltage within the range −100 to +20 mV and its polarity reversed at about −25 mV. The effects of caerulein and bombesin nonapeptide were indistinguishable from those of ACh. Voltage homogeneity in the acinar unit was attained earlier than 1 ms after a hyper- or depolarizing voltage jump. The current transients associated with voltage jumps decayed according to single exponential functions both in the absence and presence of ACh. The time constant of the single exponential current decay after a voltage jump was the same (1–3 ms) in the absence or presence of ACh. The amplitude of the current transient was, however, reduced by ACh. The time constant of the current decay following voltage jumps was independent of the voltage in the range +60 to −60 mV, both in the absence and presence of ACh. The ACh-evoked reduction in the amplitude of the transient current following voltage jumps dependend linearly on the voltage. In individual units, the slope of this curve was the same as the slope of the curve relating the steady state ACh-evoked increase in current to membrane potential. It is concluded that the ACh controlled pathways are not voltage sensitive. The effects of ACh on the current transients associated with the voltage jumps can best be explained by assuming that the ACh-evoked conductance increase resides predominantly in the lateral plasma membranes which border on narrow extracellular spaces.
    Type of Medium: Electronic Resource
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