Phonorece-ption 477 



Function: The Microphonic Effect. Movement of the hair cells against 

 the tectorial membrane gives rise to a voltage change across the sense cells. 

 The free ends of the sense cells become negative to the basal ends whenever 

 the basilar membrane is moved upward. This voltage change may be re- 

 corded from various parts of the bony structure, including the round and oval 

 windows. This voltage change of the sense cells is referred to as the "micro- 

 phonic effect" of the cochlea.''-* The microphonic effect provides a method 

 of determining the frequency sensitivity range of the cochlea of an animal. 



The microphonic effect can be distinguished from the nerve impulses by 

 a variety of criteria: a short latency of 0.1 msec, as opposed to 0.7 msec, for 

 nerve; absence of refractory period; resistance to fatigue, cold, anesthesia, and 

 ischemia; ability to follow notes close to the upper limit of hearing (16,000 

 cycles per second); and ability to follow faithfully the form of the incident 

 sound waves. These characteristics lead to the assumption that the micro- 

 phonic effect is comparable to that of an electrical transducer which passively 

 converts mechanical energy into electrical energy in very much the same 

 manner as movement of the needle in a phonograph pickup causes distortion 

 of a piezo-electric crystal, thereby producing voltage change. 



Stimulation of the Nerve. There are two theories concerning the mechan- 

 ism by which movement of the hair cells gives rise to impulses in the audi- 

 tory nerve: (1) through the microphonic effect, and (2) through a chemical 

 mediator. At present, evidence is not conclusive for either theory. 



The electrical theory assumes that the voltage of the microphonic effect is 

 the stimulating agent. Evidence for this theory consists of the fact that all 

 nerve fibers can be stimulated electrically, and the voltage of the micro- 

 phonic effect seems adequate for the purpose. The utter simplicity of this 

 explanation is most appealing. Furthermore, from a study of the timing of 

 the microphonic effect and the nerve impulses produced by a volley of sound 

 waves, it can be demonstrated that the latency of the impulse is constant only 

 if it is assumed that stimulation is associated with the negative phase of the 

 microphonic effect, i.e., when the basilar membrane is moving up and the 

 stapes out. 



Evidence that is often cited against the electrical theory is the long latent 

 period, which is usually 0.6 msec, or longer. If properties of the auditory 

 nerve are similar to those of other nerves the latency should not exceed 0.1 

 msec. If we ascribe 0. 1 msec, to latency of response and the rest of the latent 

 period to conduction time, then the rate of the impulse in the unmyelinated 

 portion of the nerve fiber (30 microns long) would be less than 10 meters 

 per second. However, there seems to be no real necessity of limiting the 

 latency to 0.1 msec. At synapses, stimulation is delayed in exactly the same 

 manner and for the same approximate times as at the sense cell-neural 

 junction in the ear, and probably for the same reason. 



The theory of a chemical mediator assumes that a chemical substance is 

 released by the sense cell under the influence of distortion in shape and that 

 this chemical substance brings about the stimulation of the nerve. This 

 theory permits one to account for the long latent period, but so far there is 

 no proof for the existence of the mediator. If this theory could be proved, 

 then the microphonic effect might be demonstrated to be purely incidental to 

 the process of stimulation. 



