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J. C. ECCLES 



Other hand, the pores are charged negatively (Fig. 9a), the membrane would 

 be selectively permeable to small cations, as occurs with crustacean stretch 

 receptor cells and vertebrate heart muscle. 



We have seen that there is a sharp separation between the permeable and 

 impermeable species of anions, and that there is virtually the same perme- 

 ability of the activated inhibitory patches for the largest permeable ion 

 (formate) as for the smallest (bromide). It may therefore be assumed that, 

 when the inhibitory transmitter acts on the membrane, it brings into existence 

 pores that have a precisely standardized size. In a personal communication 

 Fatt (1960) has suggested that such a happening could be readily envisaged 

 if the pores were permanent structures that were plugged at their external 

 opening and a transmitter molecule acted by momentarily dislodging the plug 

 as illustrated in Fig. 9c, d. For example the transmitter molecule might 

 form a bridge between two receptor sites to which it was momentarily 

 attached, one on the adjacent membrane and the other on the plug as dia- 

 grammatically shown in Fig. 9d. 



A 



B 



\ 



Fig. 9. Schematic representations of pores that are assumed to be the channels 

 for the ionic fluxes through the activated inhibitory patches on motoneurons. 

 In A the pores are negatively charged and so will be selectively permeable to small 

 cations as shown, while in b they are positively charged and so are selectively 

 permeable to small anions, as occurs with the motoneuron, c shows diagram- 

 matically the way in which an inhibitory pore is plugged, an inhibitory trans- 

 mitter molecule being shown free in the environment. In d this molecule is 

 shown in close steric relationship both to the plug and to an inhibitory receptor site 

 on the postsynaptic membrane. As aconsequence the plug has been pulled away from 

 the orifice of the pore, which is opened for the ionic flux that occurs during the 

 brief duration of the transmitter action on the subsynaptic membrane. 



In conclusion it can be stated that good explanations can now be offered 

 for the mode of action of postsynaptic inhibition in preventing the reflex 

 discharge of impulses, but there is much uncertainty in other respects. For 

 example, the central inhibitory transmitter substance is as yet unidentified 

 and one can do no more than speculate as above on the manner in which the 

 transmitter acts on the postsynaptic membrane to cause the momentary 

 appearance of pores of precisely standardized size. 



