The human body is amazing in its ability to modify external signals to maximize one's awareness, without causing excessive discomfort. Although the general mechanism of central nervous system control of sensory perception has been known, researchers at the University of Buenos Aires and the Hopkins School of Medicine only recently published a study on the cellular process at the synaptic level.
All sensory systems are capable of maximizing sensitivity to certain signals, especially in context of a noisy background. The auditory system is no exception; this is done so through feedback loops to the central nervous system.
In humans, sound waves hit the tympanic membrane, bouncing off the three bones of the middle ear, namely the malleus, incus, and stapes, finally reaching the oval window. This process amplifies the sound and transforms energy in the form of compression waves in the air to those in fluid, of which the cochlea is composed.
Traveling through the cochlea, specifically the Organ of Corti, the sound wave stimulates different areas of the basilar membrane depending on the frequency: higher frequencies resonate at the nearer stiff apex, while low frequencies reach the farther floppy base.
Next, the affected segment of the basilar membrane causes the outer hair cells, which are mechanical sensory receptors of the auditory system, to brush up against the overhead tectorial membrane, thus triggering the opening of mechanically gated potassium channels, initiating an action potential.
This signal then travels up the eighth cranial nerve, namely the vestibulochoclear nerve, through several cortex regions to process the information, and finally to the auditory cortex of the temporal lobe.
At the same time the inner hair cells are stimulated, the outer hair cells too contribute to the hearing experience. They either grow or shrink in response to incoming stimuli, thus controlling the distance between the tectorial membrane and the inner hair cells, which in turn affects one's sensitivity to sounds.
Outer hair cells are innervated by cholinergic efferent feedback from the medial portion of the superior olivary complex. These fibers are known as the medial olivocochlear fibers.
Previous studies have shown that electrical stimulation of the medial olivocochlear reduces sound-evoked motion in the cochlea and decrease in auditory nerve response, indicating that medial olivocochlear system acts to inhibit outer hair cell function. However, the mechanism at a cellular level remains largely unknown.
In this study, mouse cochleas were used. The medial olivocochlear efferent axons were stimulated. Whole cell responses of postsynaptic outer hair cells were recorded.
Results show that efferent firing frequency increases linearly with sound intensity, and is also affected by sound origin and type. This correlation suggests that short-term plasticity of the medial olivocochlear-outer hair cell synapse is involved in the graded levels of efferent feedback.
Moreover, electron micrographs of the synapse demonstrate a large number of synaptic vesicles at efferent endings. Although it is unknown as to how many are actually at the site of release, this evidence suggests that vesicle availability is not a deciding factor in determining firing frequency.
In vivo studies have shown that outer hair cell inhibition increases linearly with increased frequency of efferent fiber activation. In addition, increased medial olivocochlear fiber firing rate increases along with sound intensity. The consistency between previous in vivo studies and results from this experiment further validates the conclusions reached by the researchers.
Electrical data also suggests that only one vesicle is released upon the arrival of an action potential. Furthermore, each outer hair cell is innervated by only one efferent fiber, and each fiber rarely innervates more than one hair cell.
Statistical analysis of electrical activity at various synapses suggests that there may be variability among release sites, demonstrating a possible topic for future experimentation.
