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HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY I 



tude or the latency- Increase in rate of stimulation 

 reduces the number of spikes of the responding; neuron. 

 It has been observed, though very infrequently, 

 that the cuneate neuron may respond to peripheral 

 stimulation at a rate as high as 500 per sec. (2). 

 Evoked potentials of the thalamic neurons, which 

 receive afferent impulses after a number of synaptic 

 relays at lower levels of the neural axis, cannot follow 

 rates of stimulation even as low as 20 per sec. The 

 somatic .sensory cortex is known to be unable to 

 respond fully to peripheral stimulation at a rate 

 higher than 7 per sec. in animals under barbiturate 

 anesthesia (33); in other conditions the rate may be as 

 high as 14 per sec. (40). 



Ejjcct (if Changes in Internal and External Milicn 



The axon is generally known to withstand adverse 

 changes of the internal or external milieu better than 

 the cell body and dendrites. In accordance with this 

 tenet, the postsynaptic potential which insoKes the 

 activity of the latter structures has fjeen found to be 

 more susceptible to the lack of oxygen than the 

 presynaptic potential. In complete anoxia produced 

 by asphyxiation or by inhaling pure nitrogen, for 

 instance, the postsynaptic potential can be abolished 

 in about 90 sec. while the activity of the presynaptic 

 fibers may last for a considerably longer period of time. 

 The greatest difference between the pre- and the 

 postsynaptic potentials, however, lies in the rate of 

 recovery from anoxia. Experimental evidence shows 

 that the axonal component of the cortical response to 

 stimulation of the medullary pyramid begins to re- 

 cover from the effect of anoxia in about i min. after 

 the readmission of oxygen and resumes its original 

 size in about 5 min. The postsynaptic component of 

 the response, on the other hand, will not reappear 

 until 5 or 6 min. later. A complete recovery mav re- 

 quire even 10 or 20 min., depending on how soon 

 oxygen was readmitted (21, 22). Similarly, the 

 synaptically elicited wave (I-wave^ of the pyramidal 

 response to cortical stimulation is reduced in size 

 after 70 sec. of asphyxia and virtually aljolished after 

 130 sec, while the directly elicited di.scharges (D- 

 wave) persist Co/)- 



Like anoxia, mechanical pressure, traumatic injury 

 and low temperature all depress the postsynaptic 

 function sooner and more severely than the pre- 

 synaptic activity. There are some chemicals such as 

 strychnine and tubocurarine which may enhance 

 specifically the postsynaptic actisity without markedly 

 aflfecting the presynaptic potentials (20, 25). 



It has been observed that when the cortical surface 

 was cooled h\ controlled refrigeration, the functional 

 activity of dendrites of cortical neurons was partially 

 blocked at temperatures below 28°C and was coin- 

 pletely abolished at 22 °C;, while the functional activity 

 of axon remained without adverse changes. From this 

 fact it inay be inferred that the postsynaptic potential 

 which invokes the process of depolarization of 

 dendrites must be affected Ijy low temperature more 

 severely than the potentials deri\ed from the directly 

 excited axons (21). 



Anatomical CUnsiiIeratinns 



In determining whether or not a potential compo- 

 nent is pre- or postsynaptic, the anatomical situation 

 must be considered as a decisive factor. Obviously one 

 cannot assign a potential as postsynaptic if there are 

 only directly excited fibers present in the system in- 

 volved. In the case of antidromic action potential in 

 the optic ner\e elicited by stimulation of the optic 

 tract, for instance, it is obviously not possible to have a 

 postsynaptic component in the potentials obtained 

 (24). However, it would not be so easy to be certain 

 in a central structure which is embedded among a 

 complicated mass of \arious neural elements. In that 

 circumstance, the characteristics of the recorded 

 potential must be taken into consideration together 

 with the related anatomical organization of the system 

 concerned. An approach of this kind has been adopted 

 frequently in analysis of evoked cortical potentials. 

 We may take as an example the microelectrode study 

 of the cortical potential evoked by stimulation of the 

 ventrolateral nucleus of the thalamus (43). Recordings 

 taken from different depths of the cerebral cortex in- 

 variably show the presence of positive-negative 

 diphasic spikes in the early phase of the potential. 

 These spikes which have comparatively low voltage 

 are frequently seen at all le\els below 0.7 mm. The 

 negative phase of the spike increases as the electrode 

 is pushed deeper into the cortex. They can easily be 

 distinguished from the high voltage spikes derived 

 from the cell bodies. The short latency and the brief 

 duration of the spikes makes it certain that they are 

 from the presynaptic thalamocortical fibers which are 

 known to terminate mainly in the fourth layer of the 

 cortex located about 0.7 mm beneath the cortical 

 surface in the cat. Alignment of simultaneous re- 

 cordings from the cortical surface with a gross 

 electrode and those from the depth when a micro- 

 electrode shows a temporal coincidence of the small 

 diphasic spikes and the usual elevations of the po- 



