Joseph C. Adams, Ph.D.
Associate Professor of Otology and Laryngology, Harvard Medical School
Much of the work in my lab deals with non-sensory cells of the cochlea. This is not because sensory cells are thought to be uninteresting or even well understood, but rather because non-sensory cells are clearly essential for cochlear function and because there is growing evidence that they are often affected earlier and more severely by cochlear stresses than are sensory cells. This suggests that many poorly understood cochlear pathologies may be caused by insults that begin by compromising non-sensory cells. It is therefore reasonable to expect that the study of stress responses in non-sensory cells will lead to a better appreciation of the causes of cochlear disorders and this will provide insight into better prevention and treatment of these disorders.
Somewhat more than half the cells in the inner ear are connective tissue cells and most of these are present in the spiral ligament. The description of the distribution of the gap junction protein connexin 26 in epithelial and connective tissue cells (Kikuchi et al.), together with much previous work from other labs, convinced most cochlear researchers that K+ ions re-circulate from the perilymphatic space to the interior of the stria vascularis via gap junctions among and between fibrocytes of the spiral ligament. There is growing evidence, however, that cells within the spiral ligament have additional functions other than acting as mere conduits of K+ ions. Experiments are underway which are designed to help determine these functions.
A primary concern in this lab is with seeking ways to complement the work of the Otopathology Laboratory on basic and applied research issues. This includes efforts as disparate as optimizing tissue processing protocols and studying poorly understood cochlear cells whose malfunction may account for hearing loss. The applied research includes ongoing efforts to develop and improve techniques for processing and analyzing both newly acquired and archived temporal bones of patients who had inner ear disorders during their lives. Analyses and interpretations of these pathological specimens are aided by insights provided by results of the basic research program.
NF kappaB reporter mouse showing yellowish green type II fibrocytes that have activated NF kappaB in response to a systemic injection of the inflammatory agent LPS. The stria vascularis and type II fibrocyte regions (red) are stained for ATPase.
Click here for a searchable database of genes that are expressed in the mouse cochlea
1. Kikuchi T, Kimura RS, Paul DL, Adams JC (1995) Gap junctions in the rat cochlea: immunohistochemical and ultrastructural analysis. Anat Embryol (Berl) 191: 101-118.
2. Adams JC (2002) Clinical implications of inflammatory cytokines in the cochlea: a technical note. Otol Neurotol 23: 316-322.
3. Merchant SN, Adams JC, Nadol JB, Jr. (2005) Pathology and pathophysiology of idiopathic sudden sensorineural hearing loss. Otol. Neurotol. 26: 151-160.
4. Zehnder AF, Kristiansen AG, Adams JC, Kujawa SG, Merchant SN, McKenna, M. J. (2006) Osteoprotegerin knockout mice demonstrate abnormal remodeling of the otic capsule and progressive hearing loss. Laryngoscope 116: 201-206.
5. Griffith AJ, Yang Y, Pryor SP, Park HJ, Jabs EW, Nadol, J. B., Jr., Russell, L. J., Wasserman, D. I., Richard, G., Adams, J. C., Merchant, S. N.. (2006) Cochleosaccular dysplasia associated with a connexin 26 mutation in keratitis-ichthyosis-deafness syndrome. Laryngoscope 116: 1404-1408.
6. O'Malley JT, Merchant SN, Burgess BJ, Jones DD, Adams JC (2008) Effects of Fixative and Embedding Medium on Morphology and Immunostaining of the Cochlea. Audiol Neurootol 14: 78-87.
7. Adams JC, Seed B, Lu N, Landry A, Xavier RJ (2009) Selective activation of nuclear factor kappa B in the cochlea by sensory and inflammatory stress. Neuroscience 160(2):530-539.