Transduction of sound in the cochlea is metabolically demanding. The lateral
wall and hair cells are critically vulnerable to hypoxia, especially at high
sound levels, and tight control over cochlear blood flow (CBF) is a
physiological necessity. Yet despite the importance of CBF for hearing,
consensus on what mechanisms are involved has not been obtained.
We report on a local control mechanism for regulating inner ear blood flow
involving fibrocyte signaling. Fibrocytes in the super-strial region are
spatially distributed near pre-capillaries of the spiral ligament of the
albino guinea pig cochlear lateral wall, as demonstrably shown in
transmission electron microscope and confocal images. Immunohistochemical
techniques reveal the inter-connected fibrocytes to be positive for
Na+/K+ ATPase β1 and S100. The connected fibrocytes display
more Ca2+ signaling than other cells in the cochlear lateral
wall as indicated by fluorescence of a Ca2+ sensor, fluo-4.
Elevation of Ca2+ in fibrocytes, induced by photolytic
uncaging of the divalent ion chelator
results in propagation of a Ca2+ signal to neighboring
vascular cells and vasodilation in capillaries. Of more physiological
significance, fibrocyte to vascular cell coupled signaling was found to
mediate the sound stimulated increase in cochlear blood flow (CBF).
Cyclooxygenase-1 (COX-1) was required for capillary dilation.
The findings provide the first evidence that signaling between fibrocytes and
vascular cells modulates CBF and is a key mechanism for meeting the cellular
metabolic demand of increased sound activity.
Publisher: Public Library of Science
Date Published: 1-June-2011
Author(s): Dai M., Shi X.