Northwestern Events Calendar

Mar
13
2017

Knowles Hearing Center Speaker - Mark Rutherford - Washington University St. Louis

When: Monday, March 13, 2017
4:00 PM - 5:15 PM CT

Where: Frances Searle Building, 3-417, 2240 Campus Drive, Evanston, IL 60208 map it

Audience: Faculty/Staff - Student - Public - Post Docs/Docs - Graduate Students

Contact: Celeste Marie Lee   (847) 491-4541

Group: Knowles Hearing Center

Category: Academic

Description:

Mark A. Rutherford, Ph.D.

Washington University of St. Louis School of Medicine
Dept. of Otolaryngology-Head and Neck Surgery
Assistant Professor of Otolaryngology

Mechanisms of Sound-Induced Synaptic Disintegration in the Organ of Corti

Monday, March 13, 2017 – 4:00 pm
Evanston Campus, Frances Searle Building, Room 3-417

Activation of AMPA-type glutamate receptors may be necessary and sufficient for damage to auditory nerve fiber (ANF) terminals, as demonstrated by cochlear perfusion experiments with agonists and antogonists in vivo and in organ of Corti cell culture. In these pharmacological experiments and in response to sound, ANF postsynaptic terminals swell and burst. Current work in the Rutherford Lab is utilizing noise exposure and immunohistochemistry to study the disintegration of postsynaptic densities from presynaptic ribbons on inner hair cells (IHCs) immediately after moderate over-exposure to sound. Glutamate is recognized as the afferent neurotransmitter. Noise-induced terminal swelling (postsynaptic damage) is thought to depend on glutamate but the excitotoxic mechanisms are unknown. Presynaptic damage may depend on glutamate release, either directly or indirectly. Alternatively or additionally, trauma to the presynaptic active zone may involve mechanisms upstream of glutamate release, such as voltage-gated Ca2+ influx at the ribbon synapse. One of our goals is to understand the chemical and ionic microenvironment in the inner spiral plexus that results in dissociation of pre- and post-synaptic elements upon noise overexposure. I will present unpublished work in mice lacking the vesicular glutamate transporter-3 (Vglut3), in which many afferent synapses develop and are subsequently maintained as AMPA receptors juxtaposed with presynaptic ribbons and voltage-gated calcium channels, despite the lack of glutamatergic transmission. Lack of postsynaptic or presynaptic damage after overexposure to sound in the Vglut3 KO IHCs suggests that presynaptic Ca2+ influx alone is not sufficient and that damage to the presynaptic active zone depends on glutamate release. We studied the subunit composition of AMPA receptors on ANF terminals. At some synapses GluA2, 3, and 4 appear to occupy very similar overlapping regions. Within other synapses, the subunits appear to occupy partially non-overlapping domains. Thus, the mechanism of ANF terminal damage may involve postsynaptic calcium influx through GluA2-lacking, calcium-permeable AMPA receptors.

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