Lisa Goodrich
Harvard University, MA·Neuroscience
Hearing depends on the cochlea, the snail-shaped inner-ear organ where hair cells detect sound, and on spiral ganglion neurons (SGNs), which carry that information to the brain. Loud noise and aging can kill these cells or break their connections (synapses).
- Fields
Neuroscience
Genetics
Biology
- Topics
hearing loss
cochlea
auditory neuroscience
- Grants
- 3 known grants, through Mar 2030
What they work on
- Define how the transcription factor Gata3 controls c-Maf and Mafb through effects on chromatin, using assays of chromatin structure and subtype-specific gene expression in spiral ganglion neurons.
- Map Gata3 and Maf binding sites in each SGN subtype, and use mouse genetics to test how changing the Maf code alters neuron identity and synapse properties.
- Visualize cochlear glia and disrupt their contact with growing SGN fibers using genetic and viral tools and time-lapse imaging, to test how glia guide orderly cochlear wiring.
- Delete Gata2 from cochlear glia in mice, then measure wiring, glial maturation, neuron survival and hearing using auditory brainstem responses and otoacoustic emissions.
- Characterize how lateral olivocochlear neurons respond to noise and other stressors, and map inner ear sympathetic neurons, using viral tracing, electrophysiology and single-cell RNA sequencing.
- Test whether LOCs and IESNs act on cochlear macrophages and the immune response to protect the cochlea from noise damage, using genetic manipulation and in vivo assays in mice.
More about the research
Some people then struggle to understand speech even though they pass standard hearing tests. The lab's three projects ask, in mice, how this system is built and protected. One studies how SGN subtypes acquire their distinct synapses. Another studies how glia, support cells around neurons, help wire the cochlea. A third studies how stress-responsive neurons from outside the cochlea protect it.
Why it matters
The work could help find ways to prevent or repair hearing loss caused by noise, aging or inherited mutations. For example, it may guide efforts to regrow cochlear synapses with the right properties or to boost the ear's own stress defenses. It is also relevant to human syndromes caused by GATA2 mutations (Emberger syndrome), GATA3 mutations (HDR syndrome) and MAF mutations, as well as to glioblastoma.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Ljiljana Pasa-Tolic
University of Arizona, AZ·Biochemistry
Refine a liquid chromatography–mass spectrometry (LC-MS) proteomics platform for sensitive, high-throughput protein profiling of single spiral ganglion neurons, which relay sound from the inner ear.
Bo Hua Hu
University of Texas at Dallas, TX·Neuroscience
Determine how galectin-3, a sugar-binding immune protein, maintains hearing and cochlear structure, using mice in which the Lgals3 gene that encodes it has been disrupted.
Ian Mertes
University of Illinois Urbana-Champaign, IL·Neuroscience
Determine whether medial olivocochlear (MOC) reflex strength, measured by contralateral inhibition of otoacoustic emissions, predicts whether normal-hearing adults report difficulty understanding speech in background noise.
The school
Harvard University: 42 labs on PI Pages, $1.5B a year on research, 712 research doctorates a year.
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