Axonal sodium/potassium conductance

Figure 16.2 Saltatory conduction. Myelin acts as an insulator to prevent current loss as the action potential travels down the axon. Sodium and potassium channels are clustered at the Nodes of Ranvier, where there is no myelin. Action potentials jump from one node to the next, reducing the overall membrane area involved in conduction, and speeding up electrical transmission.

Fig.3 Effects of methanotetrametrin (pyrethroid I) on the sodium current and conductance in isolated cockroach axons. The potassium current was blocked using 0.2 mM 3,4-diaminopyridine in the external solution.

Simply put, the action potential is caused by a state of disequilibrium between ideal electrical potentials for two ions, sodium and potassium. The equilibrium potentials for Na" " and K can be thought of as the electrical force required to maintain the given ionic gradients across the cell membrane for each ion. For Na" ", the equilibrium potential is approximately 50 mV (with respect to the inside of the membrane) for K +, it is approximately —75 mV. (These values apply to the giant squid axon on which the early investigations on action potentials were conducted. Of course, these values... 

The most fundamental studies on their mode of action have been those of Narahashi who worked with giant fibre preparations. He proposed that pyrethroids modify axonal conduction within the central nervous system of insects by altering the permeability of the nerve membrane to sodium and potassium ions (Narahashi, 1965 1974 1976 Burt and Goodchild, 1977 Clements and May, 1977). 

There are no longer any experimental or logical reasons to doubt that under ordinary conditions the action potential of the squid axon membrane does indeed arise, as suggested by Hodgkin, Huxley and Katz in 1949, from the membrane conductance changes to sodium and potassium ions and the inward flow of sodium ions occurs with a time course as calculated from the equation of Hodgkin and Huxley in 1952. 

The answer is 5 III E 2J. The action potential of nerve cell membranes is depend on the instantaneous influx of sodium and efflux of potassium to initiate nerve conduction. All other mechanisms offered as possible answ s involve synaptic transmission or axonal transport but are not directly involved in generating the action potential. 

The pyrethrins act on sodium channels in the axonal membrane, decreasing and slowing inward sodium conductance and suppressing potassium outflow. They may also inhibit adenosine triphosphatases (ATPases), which may affect cation conduction at axonal membranes. The net result is decreased action potential amplitude and the generation of repetitive nerve impulses. 

When superthreshold rectangular depolarizing voltage is applied to the axon, an initial wave of inward current appears as the result of the membrane s increased permeability to sodium (the opening of sodium channels). This is followed by a wave of outward current due to the conductivity of the potassium channels. Subsequently, the outward current will correspond to the ohmic conductivity of the membrane. 

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