THOUGHTS ON INHIBITION IN THE SPINAL CORD 17 



However, in 1933, in the Nobel Lecture we find the following very up-to-date 

 thought : 



"As to inhibition the suggestion is made that it consists in the temporary stabihzation 

 of the surface-membrane which excitation would break down. . . . The inhibitory 

 stabihzation of the membrane might be pictured as a heightening of the 'resting' 

 polarization, somewhat on the lines of an electrotonus." 



The foregoing statement is non-committal as to the sort of action that 

 might bring about the postulated inhibitory stabilization, but in view of the 

 difficulties he and Eccles encountered in reconcihng their findings of 1931 

 with explanation in terms of the Wedensky effect one may suppose that an 

 humoral hypothesis was tacitly assumed the more likely. 



Mention has been made of the fact that hypotheses of indirect inhibition 

 are essentially uncommitted with respect to the precise means by which pre- 

 synaptic elements act at their terminal knobs upon subjacent tissue. There 

 exists also an hypothesis of direct inhibition annunciated by Gerard (1932) 

 and greatly elaborated by Gesell (1940), in which mode of action is un- 

 specified. Furthermore, hypothesis of direct action though it be, it is in a 

 sense allied to hypotheses of indirect action in that specifically inhibitory 

 endings are not postulated. Location on the secondary neuron of endings 

 otherwise similar in action is at the heart of this hypothesis. In brief, this 

 hypothesis holds that the motoneuron, for example, is polarized with an 

 external current flowing from axonic pole to dendritic pole. Excitation in the 

 sense of impulse formation takes place at the axon. Synapses at the dendritic 

 pole aid the current and so lead to excitation. Those at the axonic pole tend 

 to cancel the current and so lead to inhibition. 



All the general notions so far mentioned contain as part of their structure 

 the orthodox view, born of the neuron doctrine, that neurons affect other 

 neurons at their points of synaptic contact. The orthodoxy was frequently 

 imphcit, or perhaps one should say taken for granted. Nevertheless it was 

 there. One should appreciate the fact that attempts to avoid postulation of 

 specifically inhibitory synapses are not the equivalent of breaking with 

 orthodoxy as to the synaptic sites of action by one neuron upon another. 

 But there are notions concerning inliibition that do just that. And so there 

 has arisen yet a third form of dichotomy in thought. On the one hand there 

 are all the hypotheses that include inhibition as a direct synaptic action, or 

 as a consequence of direct synaptic excitatory action. On the other hand 

 there are notions of inhibition arising as a consequence of extrasynaptic 

 action. 



Such hypotheses take two forms. The first of these is associated with the 

 name of Beritoff whom I quote from a recent statement (1959): 



"Twenty-five years ago we advanced the idea that at the basis of the inhibition of the 

 nerve elements of the spinal cord and brain stem lies the electrotonic action of slow 

 potentials arising within the dendritic plexuses of the C.N.S. and first of all in the 

 3 



