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Giant squid axon

Electrophysiological protocols utilizing crayfish and squid giant axons revealed that external application of brevetoxin caused a concentration-dependent... [Pg.166]

In squid giant axons, PbTx causes a depolarization of the plasma membrane, repetitive discharges followed by depression of action potentials, and a complete blockade of excitability. This action is antagonized by TTX (83,84). PbTx depolarizes nerve terminals and induces neurotransmitter release (85,86) it depolarizes skeletal muscle cells (87) and increases the frequency of action potentials in crayfish nerve cord (88). PbTx also produces a contraction of the guinea pig ileum (89). All these effects are prevented by TTX. [Pg.195]

Much evidence supports this scheme. For example, neuronal depolarisation increases the amount of free synapsin in the cytosol and microinjection of CAM kinase II into the terminals of the squid giant axon or brain synaptosomes increases depolarisation-evoked transmitter release. By contrast, injection of dephosphorylated synapsin I into either the squid giant axon or goldfish Mauthner neurons inhibits transmitter release. [Pg.95]

Much evidence supports a role for these proteins in exocytosis. For instance, injection of recombinant SNAP into the squid giant axon increases vesicular exocytosis. Also, membrane SNAP-25 and syntaxin are both targets for botulinum toxin while the vesicule protein, synaptobrevin, is a target for tetanus and botulinum toxins both these toxins are well known for disrupting transmitter release. [Pg.97]

Hodgkin and Huxley [81] formulated a membrane model that accounts for K" ", Na" ", and ion leakage channels in squid giant axons [Fig. 22(a)]. The membrane resting potential for each ion species is treated like a battery and the degree to which the channel is open is modeled by a variable resistor. [Pg.676]

Brady, S. T., Lasek, R. J. and Allen, R. D. Fast axonal transport in extruded axoplasm from squid giant axon. Cell Mot. 3 (Video Supplement), 1983. [Pg.499]

It has been reported4 that cholinesterase inhibitors (such as di-isopropyl phosphorofluoridate) increase the permeability of squid giant axons towards sodium and potassium. There is also an indication that the erythrocyte requires, among other factors, an adequate acetylcholine-cholinesterase system to prevent a gain of sodium or a loss of potassium.5 The conclusion that permeability is dependent on cholinesterase activity, however, seems to be contested by Strickland and Thompson.6... [Pg.214]

Haydon DA, Simon AJB. 1988. Excitation of the squid giant axon by general anaesthetics. J Physiol 402 375-389. [Pg.269]

The sulfamate saxitoxins have very low potencies relative to their carbamate hydrolysis products. This relationship has been observed in every assay system tried, including the standard mouse bioassay (Figure 3), squid giant axon (1 ), frog sciatic nerve (16), mammalian brain (1 ), and single rat sarcolemma sodium channels incorporated into lipid bilayers (15). It seems unlikely that human oral potencies are an exception to this trend. [Pg.121]

The neurotoxic actions of T17 on membrane excitability were examined in squid giant axon initially and in more detail using crayfish giant axon and intracellular microelectrode techniques(14). Detailed studies utilizing T34 are not available due to technical problems associated with its extreme hydrophobicity and resulting diffi-... [Pg.361]

Preliminary testing on whole animal (bioassay) and isolated tissue preparations (voltage-clamped squid giant axons) showed effects similar to those measured for STX and neo-STX. Again the presence of anionic cryptic forms of the toxins was indicated. [Pg.404]

Haydon DA, Elliot JR, Hendry BM Effects of anesthetics on the squid giant axon in Kleinzeller A (ed) Current Topics in Membranes and Transports, vol 22. New York, Academic Press, 1984, pp 445-482. [Pg.127]

Skou had established previously that such anesthetics inhibited certain membrane-bound enzymes found in the membrane fraction isolated from nerve homogenates. He decided to study the endogenous ATPase activity as a possible target for future work, initially thinking that it might be the sodium channel. Luckily, since he lacked access to squid giant axons, he used the easily-obtained mixed nerve from the claw of the crab for this purpose. This proved to be a fortuitous choice since, in contrast to mammalian membrane fragments, these did not spontaneously reseal to form closed vesicles. This allowed substrates added to the... [Pg.258]

Figure 3. Membrane capacity (Curve I) and conductivity (Curve 2) of squid giant axon at various frequencies. Note anomalous behavior at low frequencies. Figure 3. Membrane capacity (Curve I) and conductivity (Curve 2) of squid giant axon at various frequencies. Note anomalous behavior at low frequencies.
Figure 5. Membrane capacity per unit area of squid giant axon as a function of the length of the electrodes (29) ((upper scale) electrode length in mm (lower scale) inverse of length in mm1)... Figure 5. Membrane capacity per unit area of squid giant axon as a function of the length of the electrodes (29) ((upper scale) electrode length in mm (lower scale) inverse of length in mm1)...
Figure 6. Membrane capacitance of squid giant axon at various membrane potentials. Membrane potential was shifted by injecting currents. The abscissa shows actual potential across the membrane in mV. Figure 6. Membrane capacitance of squid giant axon at various membrane potentials. Membrane potential was shifted by injecting currents. The abscissa shows actual potential across the membrane in mV.
TABLE I. The Hodgkin-Huxley equations which describe the relationship between total membrane current 1 and transmembrane potential V in the squid giant axon [see (1)]. [Pg.151]

Keynes, R. D. Rojas, E. Kinetics and steady state properties of the charged system controlling sodium conductance in the squid giant axon. J. Physiol. 1974, 239, 393-434. [Pg.159]

Meves, H. The effect of holding potential on the asymmetry currents in squid giant axons. J. Physiol. 1974, 243, 847-867. [Pg.159]

Cole, K. S. and Curtis, H. J. Electric impedance of the squid giant axon during activity. Journal of General Physiology 1939, 22 649-670. [Pg.270]

Figure 7.6 Current-voltage relationship for passive channel models of Equations (7.27) and (7.28). Sodium concentrations typical for the squid giant axon are used [Na+ ] = 437 mM [Na J = 50 mM. The sodium equilibrium potential is VNa = 58.5 mV. Conductance g a is set to 0.01 mS-cm-2. The permeability for the GHK model of Equation (7.28) is set so that both models predict the same current density at AT = 0. Figure adapted from [108],... Figure 7.6 Current-voltage relationship for passive channel models of Equations (7.27) and (7.28). Sodium concentrations typical for the squid giant axon are used [Na+ ] = 437 mM [Na J = 50 mM. The sodium equilibrium potential is VNa = 58.5 mV. Conductance g a is set to 0.01 mS-cm-2. The permeability for the GHK model of Equation (7.28) is set so that both models predict the same current density at AT = 0. Figure adapted from [108],...

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See also in sourсe #XX -- [ Pg.254 ]

See also in sourсe #XX -- [ Pg.587 ]




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Squid giant axon Hodgkins-Huxley model

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