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  • 1
    Publication Date: 1960-02-26
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 69 (1982), S. 35-40 
    ISSN: 1432-1424
    Keywords: axon ; hydrostatic pressure ; K currents ; kinetics ; activation volume
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The effect of pressure upon the delayed, K, voltage-clamp currents of giant axons from the squidLoligo vulgaris was studied in axons treated with 300nm TTX to block the early, Na, currents. The effect of TTX remained unaltered by pressure. The major change produced by pressures up to 62 MPa is a slowing down of the rising phase of the K currents by a time scaling factor which depends on pressure according to an apparent activation volume, ΔV∓, of 31 cm3/mole at 15°C; ΔV∓ increased to about 42 cm3/mole at 5°C. Pressure slightly increased the magnitude, but did not produce any obvious major change in the voltage dependence, of the steady-state K conductance estimated from the current jump at the end of step depolarizations of small amplitude (to membrane potentials,E, ≦20 mV) and relatively short duration. At higher depolarizations, pressure produced a more substantial increase of the late membrane conductance, associated with an apparent enhancement of a slow component of the K conductance which could not be described within the framework of the Hodgkin-Huxley (HH)n 4 kinetic scheme. The apparent ΔV∓ values that characterize the pressure dependence of the early component of the K conductance are very close to those that describe the effect of pressure on Na activation kinetics, and it is conceivable that they are related to activation volumes involved in the isomerization of the normal K channels. The enhancement of the slow component of membrane conductance by pressure implies either a large increase in the conductance of the ionic channels that are responsible for it or a strong relative hastening of their turn-on kinetics.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    The journal of membrane biology 69 (1982), S. 23-34 
    ISSN: 1432-1424
    Keywords: axon ; hydrostatic pressure ; Na currents ; kinetics ; temperature ; activation volume
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The effects of hydrostatic pressures up to 62 MPa upon the voltage-clamp currents of intact squid giant axons were measured using mineral oil as the pressure transmitting medium. The membrane resistance and capacitance were not appreciably affected over the whole range of pressures explored. The predominant effect of pressure is to slow the overall kinetics of the voltage-clamp currents. Both the early (Na) currents and the delayed (K) ones were slowed down by approximately the same time scale factor, which was in the range of 2 to 3 when pressure was increased from atmospheric to 62 MPa. Finer details of the effects, most evident at moderate depolarizations, are: the apparent initial delay in the turn-on of Na currents is increased by pressureless than is the phase of steepest time variation, and the later decay is slowedmore than is the rising phase. The initial time course of the currents at high pressures can be made to overlap with that at normal pressure by a constant time compression factor, Θm, together with a small, voltage-dependent delay. In a given axon, Θm was fairly independent of voltage, and it increased exponentially with pressure according to an apparent activation volume, ΔV∓, ranging between 32 and 40 cm3/mole. ΔV∓ tended to decrease with increasing temperature. Contrary to what is observed for moderate or large depolarizations, the kinetics of Na inactivation produced by conditioning prepulses of −50 or −60 mV was little affected over the whole range of pressures explored. Inferences about the pressure dependence of the steady-state Na activation were made from the comparison of the plots of early peak currents,I p, versus membrane potential,E. The Na reversal potential,E Na, and the slope of the plots nearE Na did not change significantly with pressure, but the peak Na conductancevs. E relationship was shifted by about +9 mV upon increasing pressure to 62 MPa. Steady-state Na inactivation,h ∞, was slightly affected by pressure. At 62 MPa the midpoint potential of theh ∞ (E) curve,E h, was shifted negatively by about 4 mV, while the slope atE h decreased by about 38%. Under the tentative assumption that pressure directly affects the gating of Na channels, the Na activation data follows a simple Hodgkin-Huxley scheme if the opening of anm gate involves an activation volume of about 58 Å3 and a net volume increase of about 26 Å3. However, a self-consistent description of the totality of the effects of pressure on Na inactivation cannot be obtained within a similar simple context.
    Type of Medium: Electronic Resource
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