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Figure 1. Diagram of “set point adjustment” by lateral olivocochlear efferent (E) innervation of the afferent peripheral processes (A) of type I spiral ganglion cells. The efferent terminal on the left is more likely to release the excitatory (++) transmitters Acetylcholine (ACh), Dynorphin (Dyn), or Calcitonin Gene-Related Peptide (CGRP) which act at the post-synaptic ACh receptor (AChR) or neuropeptide receptors (NPR) in the afferent terminal. The resulting depolarization raises the resting potential within the terminal and lowers (arrow down) the “set point”, making the excitatory (++) action of glutamate (Glu) released from the Inner Hair Cell more effective at the glutamate receptors (GluRs). Efficacy can also be enhanced by increasing the number of GluRs placed into the membranous pool from the cytoplasmic pool (double arrow). The efferent terminal on the right is more likely to release the inhibitory (—) transmitters Dopamine (Dop), Enkephalin (Enk) and ã-aminobutyric acid (GABA), which act at the post-synaptic GABA receptor (GABAR) or neuropeptide receptors (NPR) in the Afferent terminal. The hyperpolarization decreases the resting potential within the terminal and raises (arrow up) the set point, making the excitatory (++) action of glutamate (Glu) released from the Inner Hair Cell less effective at GluRs. This efficacy can also be lowered by decreasing the number of GluRs from the cytoplasmic pool that are placed into the membranous pool (double arrow).

Figure 1. Diagram of “set point adjustment” by lateral olivocochlear efferent (E) innervation of the
afferent peripheral processes (A) of type I spiral ganglion cells. The efferent terminal on the left is more
likely to release the excitatory (++) transmitters Acetylcholine (ACh), Dynorphin (Dyn), or Calcitonin
Gene-Related Peptide (CGRP) which act at the post-synaptic ACh receptor (AChR) or neuropeptide
receptors (NPR) in the afferent terminal. The resulting depolarization raises the resting potential
within the terminal and lowers (arrow down) the “set point”, making the excitatory (++) action of
glutamate (Glu) released from the Inner Hair Cell more effective at the glutamate receptors (GluRs).
Efficacy can also be enhanced by increasing the number of GluRs placed into the membranous pool
from the cytoplasmic pool (double arrow). The efferent terminal on the right is more likely to release
the inhibitory (—) transmitters Dopamine (Dop), Enkephalin (Enk) and ã-aminobutyric acid (GABA),
which act at the post-synaptic GABA receptor (GABAR) or neuropeptide receptors (NPR) in the
Afferent terminal. The hyperpolarization decreases the resting potential within the terminal and raises
(arrow up) the set point, making the excitatory (++) action of glutamate (Glu) released from the Inner
Hair Cell less effective at GluRs. This efficacy can also be lowered by decreasing the number of GluRs
from the cytoplasmic pool that are placed into the membranous pool (double arrow).