EXCITATION, INHIBITION 

 AND THE CONCEPT OF THE STIMULUS 



Ernst Florey 



Department of Zoology, University of Washington, Seattle 5, Washington 



Inhibition is not confined to the central nervous system and to the peripheral 

 innervation of cardiac and striated muscle (crustacea) but occurs also with 

 sensory receptor neurons. Here the phenomenon of inhibition can have two 

 causes: (1) the action of efferent inhibitory neurons, and (2) the "rebound" 

 (silent period) which immediately follows the cessation of excitatory stimula- 

 tion to which the neuron has accommodated. Efferent inhibitory neurons and 

 inhibitory agents can produce two effects on the receptor neurons: (1) temp- 

 orary depression or inhibition of excitability during the direct action of the 

 inhibitory agent (neuron); and (2) "rebound" excitation which occurs when 

 the inhibitory action suddenly ceases. It is the second effect of inhibitory agents 

 to which I wish to draw attention, because this appears to be a functionally 

 most important mechanism which does not depend on inhibitory neurons or 

 synaptic inhibition. Although the phenomenon can best be studied in sensory 

 receptor neurons it is likely to play a major role in the functioning of central 

 neurons. 



I could not resist to show once more the famous figure (Fig. 1) of Eyzaguirre 

 and Kufi^er (1955) which demonstrates that in the crayfish stretch receptor 

 neuron stretch causes depolarization and that the frequency of firing of the 

 neuron is proportional to the amount of membrane depolarization. The 

 record shown in this figure, furthermore, shows that during maintained 

 stretch the impulse frequency falls off (adaptation) and that simultaneously 

 the membrane depolarization is diminished {accomnwdation). It can also be 

 seen that at the end of stretch stimulation, that is at the moment when the 

 muscle element is allowed to relax to its original length, there occurs a 

 momentary hyperpolarization : the membrane potential becomes for a 

 moment larger than the equilibrium potential which corresponds to the 

 particular resting tension of the receptor muscle. The exact opposite happens 

 when the tension of the receptor muscle is lowered for a period of time and 

 then suddenly raised to its original value. In this case the rise in tension 

 causes the membrane potential to swing temporarily below the equifibrium 

 potential. This transient depolarization can be sufficient to set off one or a 



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