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J Dudel - One of the best experts on this subject based on the ideXlab platform.

  • open channel and competitive block of the embryonic form of the nicotinic receptor of mouse myotubes by tubocurarine
    The Journal of Physiology, 1996
    Co-Authors: Johannes Bufler, C Franke, H Parnas, R Wilhelm, J Dudel
    Abstract:

    1. Embryonic-like nicotinic channels were studied in mouse myotubes. Channel currents were measured by patch clamping outside-out excised patches to which pulses of agonists and drugs could be applied by a liquid filament switch. The holding potential of the patches was generally around-10 to-40 mV. 2. Pulses of 100 microM or 1 mM acetylcholine (ACh) elicited average channel currents which reached a maximum open probability of 0.93 within 0.5-1.0 ms, decayed with a time constant of desensitization of 20-80 ms, and fell rapidly to zero at the end of the pulse. When such pulses together with increasing concentrations of (+)-tubocurarine (TC) were applied to outside-out patches, the time constant of current decay, tau, decreased beginning at concentrations of TC added to the test solution of > 10 microM, and the peak amplitude of the current decreased markedly at concentrations of TC of > 30 microM due to an open channel block of nicotinic channels by TC. 3. When the outside-out patches were pre-incubated with TC, the peak current elicited by pulses of 100 microM ACh or 1 mM ACh + TC decreased markedly, beginning with concentrations of TC > 30 nM due to a competitive block. 4. The results could be quantitatively modelled by computer calculations based on a Circular Reaction scheme containing desensitization. TC blocked the open state as well as the unliganded closed state of the embryonic-like nicotinic receptors of mouse myotubes. Also the blocked open channel was subject to desensitization. 5. The rates of block and unblock of the open channel were 3 x 10(6) M-1 S-1 and 0.8 S-1, respectively, and those of the competitive block were 0.5 x 10(6) M-1 S-1 and 0.1 S-1, respectively (at 20 degrees C).

  • open channel block by physostigmine and procaine in embryonic like nicotinic receptors of mouse muscle
    European Journal of Neuroscience, 1996
    Co-Authors: Johannes Bufler, C Franke, H Parnas, J Dudel
    Abstract:

    Embryonic-like nicotinic channels were studied in mouse myotubes. Channel currents were measured by patch-clamping outside-out excised patches to which pulses of agonists and drugs could be applied by a liquid filament switch. The holding potential of the patches was generally around 40 mV. Pulses of 10(-4) M acetylcholine elicited average channel currents which reached a peak open probability, P(o,peak,) of 0.93 within 0.5 ms and decayed with a time constant of desensitization of 20-80 ms. When physostigmine (10(-5) to 10(-3) M) or procaine (3 x 10(-5) to 10(-3) M) was added to the acetylcholine pulses, a fast decay component of the current appeared which shortened to a time constant of 0.5 ms for the maximal drug concentrations. The fast decay was followed by a slow one which declined in amplitude with increasing concentrations of the drugs. After the end of pulses of 10 M acetylcholine plus 3 x 10(-4) M physostigmine the average current rose again, reaching a peak with approximately 5 ms delay, and then decayed slowly. The amplitude of this recovery current was approximately 0.4 P(o,peak) after 5 ms pulses and decreased with increasing pulse duration due to desensitization. The results can be quantitatively modelled based on a Circular Reaction scheme involving desensitization. Physostigmine and procaine bind to the open state to cause channel block. Also, the blocked channel was subject to desensitization. The rate constants of block were 6 x 10(6) M(-1) s(-1) for physostigmine and 2 x 10(6) M(-1) s(-1) for procaine, and the rate of unblocking was 200 s(-1) for both blockers (at -40 mV and 20 degrees C).

Johannes Bufler - One of the best experts on this subject based on the ideXlab platform.

  • open channel and competitive block of the embryonic form of the nicotinic receptor of mouse myotubes by tubocurarine
    The Journal of Physiology, 1996
    Co-Authors: Johannes Bufler, C Franke, H Parnas, R Wilhelm, J Dudel
    Abstract:

    1. Embryonic-like nicotinic channels were studied in mouse myotubes. Channel currents were measured by patch clamping outside-out excised patches to which pulses of agonists and drugs could be applied by a liquid filament switch. The holding potential of the patches was generally around-10 to-40 mV. 2. Pulses of 100 microM or 1 mM acetylcholine (ACh) elicited average channel currents which reached a maximum open probability of 0.93 within 0.5-1.0 ms, decayed with a time constant of desensitization of 20-80 ms, and fell rapidly to zero at the end of the pulse. When such pulses together with increasing concentrations of (+)-tubocurarine (TC) were applied to outside-out patches, the time constant of current decay, tau, decreased beginning at concentrations of TC added to the test solution of > 10 microM, and the peak amplitude of the current decreased markedly at concentrations of TC of > 30 microM due to an open channel block of nicotinic channels by TC. 3. When the outside-out patches were pre-incubated with TC, the peak current elicited by pulses of 100 microM ACh or 1 mM ACh + TC decreased markedly, beginning with concentrations of TC > 30 nM due to a competitive block. 4. The results could be quantitatively modelled by computer calculations based on a Circular Reaction scheme containing desensitization. TC blocked the open state as well as the unliganded closed state of the embryonic-like nicotinic receptors of mouse myotubes. Also the blocked open channel was subject to desensitization. 5. The rates of block and unblock of the open channel were 3 x 10(6) M-1 S-1 and 0.8 S-1, respectively, and those of the competitive block were 0.5 x 10(6) M-1 S-1 and 0.1 S-1, respectively (at 20 degrees C).

  • open channel block by physostigmine and procaine in embryonic like nicotinic receptors of mouse muscle
    European Journal of Neuroscience, 1996
    Co-Authors: Johannes Bufler, C Franke, H Parnas, J Dudel
    Abstract:

    Embryonic-like nicotinic channels were studied in mouse myotubes. Channel currents were measured by patch-clamping outside-out excised patches to which pulses of agonists and drugs could be applied by a liquid filament switch. The holding potential of the patches was generally around 40 mV. Pulses of 10(-4) M acetylcholine elicited average channel currents which reached a peak open probability, P(o,peak,) of 0.93 within 0.5 ms and decayed with a time constant of desensitization of 20-80 ms. When physostigmine (10(-5) to 10(-3) M) or procaine (3 x 10(-5) to 10(-3) M) was added to the acetylcholine pulses, a fast decay component of the current appeared which shortened to a time constant of 0.5 ms for the maximal drug concentrations. The fast decay was followed by a slow one which declined in amplitude with increasing concentrations of the drugs. After the end of pulses of 10 M acetylcholine plus 3 x 10(-4) M physostigmine the average current rose again, reaching a peak with approximately 5 ms delay, and then decayed slowly. The amplitude of this recovery current was approximately 0.4 P(o,peak) after 5 ms pulses and decreased with increasing pulse duration due to desensitization. The results can be quantitatively modelled based on a Circular Reaction scheme involving desensitization. Physostigmine and procaine bind to the open state to cause channel block. Also, the blocked channel was subject to desensitization. The rate constants of block were 6 x 10(6) M(-1) s(-1) for physostigmine and 2 x 10(6) M(-1) s(-1) for procaine, and the rate of unblocking was 200 s(-1) for both blockers (at -40 mV and 20 degrees C).

C Franke - One of the best experts on this subject based on the ideXlab platform.

  • open channel and competitive block of the embryonic form of the nicotinic receptor of mouse myotubes by tubocurarine
    The Journal of Physiology, 1996
    Co-Authors: Johannes Bufler, C Franke, H Parnas, R Wilhelm, J Dudel
    Abstract:

    1. Embryonic-like nicotinic channels were studied in mouse myotubes. Channel currents were measured by patch clamping outside-out excised patches to which pulses of agonists and drugs could be applied by a liquid filament switch. The holding potential of the patches was generally around-10 to-40 mV. 2. Pulses of 100 microM or 1 mM acetylcholine (ACh) elicited average channel currents which reached a maximum open probability of 0.93 within 0.5-1.0 ms, decayed with a time constant of desensitization of 20-80 ms, and fell rapidly to zero at the end of the pulse. When such pulses together with increasing concentrations of (+)-tubocurarine (TC) were applied to outside-out patches, the time constant of current decay, tau, decreased beginning at concentrations of TC added to the test solution of > 10 microM, and the peak amplitude of the current decreased markedly at concentrations of TC of > 30 microM due to an open channel block of nicotinic channels by TC. 3. When the outside-out patches were pre-incubated with TC, the peak current elicited by pulses of 100 microM ACh or 1 mM ACh + TC decreased markedly, beginning with concentrations of TC > 30 nM due to a competitive block. 4. The results could be quantitatively modelled by computer calculations based on a Circular Reaction scheme containing desensitization. TC blocked the open state as well as the unliganded closed state of the embryonic-like nicotinic receptors of mouse myotubes. Also the blocked open channel was subject to desensitization. 5. The rates of block and unblock of the open channel were 3 x 10(6) M-1 S-1 and 0.8 S-1, respectively, and those of the competitive block were 0.5 x 10(6) M-1 S-1 and 0.1 S-1, respectively (at 20 degrees C).

  • open channel block by physostigmine and procaine in embryonic like nicotinic receptors of mouse muscle
    European Journal of Neuroscience, 1996
    Co-Authors: Johannes Bufler, C Franke, H Parnas, J Dudel
    Abstract:

    Embryonic-like nicotinic channels were studied in mouse myotubes. Channel currents were measured by patch-clamping outside-out excised patches to which pulses of agonists and drugs could be applied by a liquid filament switch. The holding potential of the patches was generally around 40 mV. Pulses of 10(-4) M acetylcholine elicited average channel currents which reached a peak open probability, P(o,peak,) of 0.93 within 0.5 ms and decayed with a time constant of desensitization of 20-80 ms. When physostigmine (10(-5) to 10(-3) M) or procaine (3 x 10(-5) to 10(-3) M) was added to the acetylcholine pulses, a fast decay component of the current appeared which shortened to a time constant of 0.5 ms for the maximal drug concentrations. The fast decay was followed by a slow one which declined in amplitude with increasing concentrations of the drugs. After the end of pulses of 10 M acetylcholine plus 3 x 10(-4) M physostigmine the average current rose again, reaching a peak with approximately 5 ms delay, and then decayed slowly. The amplitude of this recovery current was approximately 0.4 P(o,peak) after 5 ms pulses and decreased with increasing pulse duration due to desensitization. The results can be quantitatively modelled based on a Circular Reaction scheme involving desensitization. Physostigmine and procaine bind to the open state to cause channel block. Also, the blocked channel was subject to desensitization. The rate constants of block were 6 x 10(6) M(-1) s(-1) for physostigmine and 2 x 10(6) M(-1) s(-1) for procaine, and the rate of unblocking was 200 s(-1) for both blockers (at -40 mV and 20 degrees C).

H Parnas - One of the best experts on this subject based on the ideXlab platform.

  • open channel and competitive block of the embryonic form of the nicotinic receptor of mouse myotubes by tubocurarine
    The Journal of Physiology, 1996
    Co-Authors: Johannes Bufler, C Franke, H Parnas, R Wilhelm, J Dudel
    Abstract:

    1. Embryonic-like nicotinic channels were studied in mouse myotubes. Channel currents were measured by patch clamping outside-out excised patches to which pulses of agonists and drugs could be applied by a liquid filament switch. The holding potential of the patches was generally around-10 to-40 mV. 2. Pulses of 100 microM or 1 mM acetylcholine (ACh) elicited average channel currents which reached a maximum open probability of 0.93 within 0.5-1.0 ms, decayed with a time constant of desensitization of 20-80 ms, and fell rapidly to zero at the end of the pulse. When such pulses together with increasing concentrations of (+)-tubocurarine (TC) were applied to outside-out patches, the time constant of current decay, tau, decreased beginning at concentrations of TC added to the test solution of > 10 microM, and the peak amplitude of the current decreased markedly at concentrations of TC of > 30 microM due to an open channel block of nicotinic channels by TC. 3. When the outside-out patches were pre-incubated with TC, the peak current elicited by pulses of 100 microM ACh or 1 mM ACh + TC decreased markedly, beginning with concentrations of TC > 30 nM due to a competitive block. 4. The results could be quantitatively modelled by computer calculations based on a Circular Reaction scheme containing desensitization. TC blocked the open state as well as the unliganded closed state of the embryonic-like nicotinic receptors of mouse myotubes. Also the blocked open channel was subject to desensitization. 5. The rates of block and unblock of the open channel were 3 x 10(6) M-1 S-1 and 0.8 S-1, respectively, and those of the competitive block were 0.5 x 10(6) M-1 S-1 and 0.1 S-1, respectively (at 20 degrees C).

  • open channel block by physostigmine and procaine in embryonic like nicotinic receptors of mouse muscle
    European Journal of Neuroscience, 1996
    Co-Authors: Johannes Bufler, C Franke, H Parnas, J Dudel
    Abstract:

    Embryonic-like nicotinic channels were studied in mouse myotubes. Channel currents were measured by patch-clamping outside-out excised patches to which pulses of agonists and drugs could be applied by a liquid filament switch. The holding potential of the patches was generally around 40 mV. Pulses of 10(-4) M acetylcholine elicited average channel currents which reached a peak open probability, P(o,peak,) of 0.93 within 0.5 ms and decayed with a time constant of desensitization of 20-80 ms. When physostigmine (10(-5) to 10(-3) M) or procaine (3 x 10(-5) to 10(-3) M) was added to the acetylcholine pulses, a fast decay component of the current appeared which shortened to a time constant of 0.5 ms for the maximal drug concentrations. The fast decay was followed by a slow one which declined in amplitude with increasing concentrations of the drugs. After the end of pulses of 10 M acetylcholine plus 3 x 10(-4) M physostigmine the average current rose again, reaching a peak with approximately 5 ms delay, and then decayed slowly. The amplitude of this recovery current was approximately 0.4 P(o,peak) after 5 ms pulses and decreased with increasing pulse duration due to desensitization. The results can be quantitatively modelled based on a Circular Reaction scheme involving desensitization. Physostigmine and procaine bind to the open state to cause channel block. Also, the blocked channel was subject to desensitization. The rate constants of block were 6 x 10(6) M(-1) s(-1) for physostigmine and 2 x 10(6) M(-1) s(-1) for procaine, and the rate of unblocking was 200 s(-1) for both blockers (at -40 mV and 20 degrees C).

Alexei A. Lapkin - One of the best experts on this subject based on the ideXlab platform.

  • Modelling Circular Structures in Reaction Networks: Petri Nets and Reaction Network Flux Analysis
    Computer Aided Chemical Engineering, 2020
    Co-Authors: Jana M. Weber, Artur M. Schweidtmann, Eduardo Nolasco, Alexei A. Lapkin
    Abstract:

    Abstract Optimal Reaction pathways for the conversion of renewable feedstocks are often examined by Reaction network flux analysis. An alternative modelling approach for Reaction networks is a Petri net. These explicitly take the Reaction sequence into account. In the optimisation of a network, this can allow the implementation of constraints on Circular Reaction structures, which are common substructures in chemical Reaction networks. In this study, we compare the performance of the models in an illustrative minimal working example of a Circular Reaction substructure. The Reaction network flux analysis is shown to be a relaxation of the Petri net formulation. Most notable, this work contributes to well-reasoned model choices for Reaction networks.