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Extra info for Reviews of Physiology, Biochemistry and Pharmacology 133
Km. ,,, R* ( :,0< k~ )O*( )0< (3) > k~. < ) I* 38 W. , R, O, and I), a feature not included in Scheme 3. In complementary experiments on frog nerve fibers Rando (1989) studied the recovery of peak current and the decrease in the "late" current after a series of impulses. This process was clearly faster (complete within 20 s) than the former, which developed in two phases. , in the P state, since modified "resting" channels would be conducting at the holding potential (see Sect. 2). Rando (1989) emphasizes the special nature of I x in this context (being favored by more negative potentials); he proposes that the slow current tails on repolarization are caused by a very slow O~-I x transition and not by the dissociation of veratridine from the channel.
Thus in frog nodes of Ranvier shifts of holding potential between -50 and -90 mV does not influence block by TTX (Ulbricht and Wagner 1975) nor is block by STX affected by a change in test pulse frequency from 1 to 10 Hz (Wagner and Ulbricht 1976). 8 Hz) intensifies block by both TTX and STX during the trains of pulses (L6nnendonker 1989). Other authors report no such use dependence of STX block in Ranvier nodes unless the membrane is pretreated with batrachotoxin, possibly because STX binding to (maintained) open channels is voltage dependent (Rando and Strichartz 1986), as has been suggested for TTX binding to modified brain Na + channels (Wang and Wang 1994).
The results show that positive cooperativity between veratridine and ATX II, which is observed only at negative membrane potentials, results from channel gating but not from conductance changes. Interestingly, the midpoint potential of the overall fractional open time in the mixture is shifted markedly to more negative membrane potentials than in either veratridine or ATX II alone. In cultured cardiomyocytes the artificial coactivator S-DPI 201-106 (possibly binding to a site different from that for ATX II; Scholtysik et al.