110 ERNST TLOREY AND GRAHAM HOYLE 



several muscle fibers large spikes (60 mV) were elicited by the summated 

 potentials (Fig. 5) although none was present in the untreated preparation 

 even with the highest possible stimulation rate. 



In our experience, picrotoxin did not prevent GABA from attenuating 

 excitatory junctional potentials, i.e. the two substances were not antagonistic 

 to each other for these crabs. If applied in more dilute solution, picrotoxin 

 (I0~5 g/ml) did prevent the inhibition of tension development during stimu- 

 lation of the inhibitory fiber. 



DISCUSSION 



The results obtained stand in marked contrast to those obtained from 

 lobsters. The principal difference is that in the crabs neither GABA nor the 

 natural inhibitory transmitter substance cause more than a minute resistance 

 change. It might be that this is due to there being a much smaller subsynaptic 

 membrane area in the crabs, or there might be a genuine smaller permeability 

 change. The marked attenuation of the junctional potentials caused by 

 GABA, as compared with the lack of a-inhibition, means that normal in- 

 hibition causes a mechanical inhibition in a different way than GABA. The 

 latter clearly acts by reducing excitatory transmitter action, either as a result 

 of competition for receptor molecules or by reducing the quantity of trans- 

 mitter released per impulse. 



The failure of the natural inhibitory transmitter substance to cause attenu- 

 ation of the junctional potentials is probably explained by the small resistance 

 change caused by it in the subsynaptic area. This highlights the problem of 

 the true nature of the action of the normal inhibitory transmitter. Since this 

 is not associated with attenuation of junctional potentials it must be due 

 either to the slight repolarization which causes a faster rate of decay of 

 potentials or to a later action in the chain of events couphng excitation to 

 contraction. 



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