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J G Starkus

Publications and source records attributed to J G Starkus.

20 records · Page 2Linked to original sources

Sensitivity of excitable and inexcitable membranes to alpha-dihydrograyanotoxin II.

A variety of excitable and inexcitable preparations have been examined for their sensitivity to the depolarizing action of alpha-dihydrograyanotoxin II. alpha-Dihydrograyanotoxin II was effective in producing membrane depolarization in giant axons from the crayfish (Procambarus clarki) and sartorius muscle fibers from the frog (Rana pipiens) and the salamander (Taricha torosa). The toxin-induced depolarization was reversed by lowering the external sodium concentration. High concentrations of tetrodotoxin and saxitoxin were also effective in reversing the depolarization in the various grayanotoxin-sensitive preparations studied except in the salamander sartorius muscle, in which sodium-dependent action potentials were highly resistant to tetrodotoxin and saxitoxin. In contrast, alpha-dihydrograyanotoxin II was ineffective in changing the resting membrane potential in the muscle fibers of the crayfish (Procambarus clarki and Orconectes virilis) and in the salivary gland giant cells from Drosophila virilis. Of the preparations that were examined, only the membranes that produce a sodium-dependent action potential are sensitive to the depolarizing action of alpha-dihydrograyanotoxin II.

Action Potentials↗

Modification of slow sodium inactivation in nerve after internal perfusion with trypsin.

Crayfish axons, internally perfused and held at depolarized membrane potentials, exhibit an inactivation of sodium conductance with slow kinetics. Restoration of maximum peak early currents requires prepulse hyperpolarizations of up to 1 s duration. Addition of trypsin to the internal perfusate at low concentrations (0.02 mg/ml) causes a rapid and irreversible loss of slow inactivation at the resting potential and a corresponding increase in Na currents to maximum values. After trypsin action, steady-state slow Na inactivation is shifted by 20--25 mV in the depolarizing direction, with no change in fast (h) inactivation. N-ethylmaleimide (NEM), a reagent with a high specificity for sulfhydryl groups, has been shown to induce slow inactivation, modify fast inactivation, and block a fraction of the Na conductance. After trypsin action NEM no longer increases slow Na inactivation but other effects remain. Prior exposure to NEM does not protect axons against the loss of slow inactivation caused by trypsin.

Animals↗