Gating of sodium and potassium channels

Bezanilla, Francisco

doi:10.1007/bf01868424

Cited by 98 publications

(56 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The slowing down of action potential repolarization by BDM may result from the phosphatase-like ability of BDM to oppose phosphorylation of the delayed rectifier K+ channel, resulting in a decreased K+ conductance during delayed rectification. This suggestion is supported by Bezanilla, DiPolo, Caputo, Rojas & Torres (1985) and Bezanilla (1985), who showed that a phosphorylation step is involved in delayed rectification in the squid axon, and Coulombe et al (1990), who showed that BDM inhibits transient outward currents in rat ventricular myocytes. However, Fryer et al (1988 a, b) found that BDM had no effect on the electrical properties of action potentials and failed to potentiate or prolong twitch aequorin light responses in rat twitch muscle, suggesting that there are species-specific differences in the channel properties involved in action potential generation in amphibian and mammalian skeletal muscle.…”

Section: Resultsmentioning

confidence: 73%

Contractile activation and measurements of intracellular Ca2+ concentration in cane toad twitch fibres in the presence of 2,3‐butanedione monoxime

Lyster¹,

Stephenson²

1995

Experimental Physiology

View full text Add to dashboard Cite

SUMMARYThe effects of 2,3-butanedione monoxime (BDM, 0 5-20 mM) on Ca2+-activated force in skinned muscle fibres, and force and Ca2+ responses in aequorin-injected intact fibres from the iliofibularis muscle of the cane toad Bufo marinus were investigated. Peak twitch force responses progressively decreased to 3 % of the control response with increasing [BDM] [Ca2+] at different concentrations of BDM. In 10 mm BDM, the rate of force development in intact fibres was slower by a factor of two at saturating [Ca2+], and was up to one order of magnitude slower at non-saturating [Ca2+], when compared with control responses. At a similar intracellular [Ca2+] steady-state isometric force was reduced to about 85 and 50 % of the control responses in 2 and 10 mm BDM, respectively. The effect of BDM on maximum Ca2+-activated force in skinned fibres paralleled the decrease in tetanic (170 Hz) force observed in intact fibres. The rate of force development in skinned fibres decreased with an increase in [BDM] at constant [Ca2+], and the sensitivity of the contractile apparatus to Ca2+ was shifted to a higher [Ca2+] by BDM. The results suggest that BDM reduces contractility in cane toad iliofibularis muscle by direct inhibition of the contractile apparatus, and reduction of the release of activator Ca2+ from the sarcoplasmic reticulum. Furthermore, BDM may be a useful tool to help study the relationship between force and [Ca2+] in intact muscle fibres.

show abstract

Section: Resultsmentioning

confidence: 73%

Contractile activation and measurements of intracellular Ca2+ concentration in cane toad twitch fibres in the presence of 2,3‐butanedione monoxime

Lyster¹,

Stephenson²

1995

Experimental Physiology

View full text Add to dashboard Cite

show abstract

“…First, in the Hodgkin-Huxley model, activation and inactivation are kinetically independent. This independence has been shown to be untenable on the basis of gating and ion current measurements in the squid giant axon (Armstrong, 1981;Bezanilla, 1985). Consequently, Markov models that are required to reproduce gating currents, such as the Vandenberg-Bezanilla model examined here, require schemes with coupled activation and inactivation.…”

Section: Voltage-gated Lon Channelsmentioning

confidence: 99%

Synthesis of models for excitable membranes, synaptic transmission and neuromodulation using a common kinetic formalism

1994

View full text Add to dashboard Cite

Markov kinetic models were used to synthesize a complete description of synaptic transmission, including opening of voltage-dependent channels in the presynaptic terminal, release of neurotransmitter, gating of postsynaptic receptors, and activation of second-messenger systems. These kinetic schemes provide a more general framework for modeling ion channels than the Hodgkin-Huxley formalism, supporting a continuous spectrum of descriptions ranging from the very simple and computationally efficient to the highly complex and biophysically precise. Examples are given of simple kinetic schemes based on fits to experimental data that capture the essential properties of voltage-gated, synaptic and neuromodulatory currents. The Markov formalism allows the dynamics of ionic currents to be considered naturally in the larger context of biochemical signal transduction. This frame, work can facilitate the integration of a wide range of experimental data and promote consistent theoretical analysis of neural mechanisms from molecular interactions to network computations.

show abstract

“…As indicated previously, to account for this we have used the previously described modified Hodgkin-Huxley (1952) scheme with a voltage-dependent activation parameter raised to a power of 2 to model this current change (cf. Bezanilla, 1985;DiFrancesco, 1985). The onset of the current can be fitted using the expression:…”

Section: Time Dependence Of Ifmentioning

confidence: 99%

Voltage clamp measurements of the hyperpolarization‐activated inward current I(f) in single cells from rabbit sino‐atrial node.

Ginneken

Giles

1991

The Journal of Physiology

120

121

View full text Add to dashboard Cite

Gating of sodium and potassium channels

Cited by 98 publications

References 54 publications

Contractile activation and measurements of intracellular Ca2+ concentration in cane toad twitch fibres in the presence of 2,3‐butanedione monoxime

Contractile activation and measurements of intracellular Ca2+ concentration in cane toad twitch fibres in the presence of 2,3‐butanedione monoxime

Synthesis of models for excitable membranes, synaptic transmission and neuromodulation using a common kinetic formalism

Voltage clamp measurements of the hyperpolarization‐activated inward current I(f) in single cells from rabbit sino‐atrial node.

Contact Info

Product

Resources

About