Deletion of Shank1 has minimal effects on the molecular composition and function of glutamatergic afferent postsynapses in the mouse inner ear

Jeremy P. Braude, Sarath Vijayakumar, Katherine Baumgarner, Rebecca Laurine, Timothy A Jones, Sherri M Jones, Sonja J. Pyott

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Shank proteins (1-3) are considered the master organizers of glutamatergic postsynaptic densities in the central nervous system, and the genetic deletion of either Shank1, 2, or 3 results in altered composition, form, and strength of glutamatergic postsynapses. To investigate the contribution of Shank proteins to glutamatergic afferent synapses of the inner ear and especially cochlea, we used immunofluorescence and quantitative real time PCR to determine the expression of Shank1, 2, and 3 in the cochlea. Because we found evidence for expression of Shank1 but not 2 and 3, we investigated the morphology, composition, and function of afferent postsynaptic densities from defined tonotopic regions in the cochlea of Shank1-/- mice. Using immunofluorescence, we identified subtle changes in the morphology and composition (but not number and localization) of cochlear afferent postsynaptic densities at the lower frequency region (8kHz) in Shank1-/- mice compared to Shank1+/+ littermates. However, we detected no differences in auditory brainstem responses at matching or higher frequencies. We also identified Shank1 in the vestibular afferent postsynaptic densities, but detected no differences in vestibular sensory evoked potentials in Shank1-/- mice compared to Shank1+/+ littermates. This work suggests that Shank proteins play a different role in the development and maintenance of glutamatergic afferent synapses in the inner ear compared to the central nervous system.

Original languageEnglish (US)
Pages (from-to)52-64
Number of pages13
JournalHearing Research
Volume321
DOIs
StatePublished - Mar 1 2015

Fingerprint

Post-Synaptic Density
Cochlea
Inner Ear
Synapses
Fluorescent Antibody Technique
Central Nervous System
Proteins
Brain Stem Auditory Evoked Potentials
Evoked Potentials
Real-Time Polymerase Chain Reaction
Maintenance

Keywords

  • ABR
  • AMPAR
  • CNS
  • CTBP2
  • DIC
  • GKAP
  • IHC
  • PSD
  • VsEPs

ASJC Scopus subject areas

  • Sensory Systems
  • Medicine(all)

Cite this

Deletion of Shank1 has minimal effects on the molecular composition and function of glutamatergic afferent postsynapses in the mouse inner ear. / Braude, Jeremy P.; Vijayakumar, Sarath; Baumgarner, Katherine; Laurine, Rebecca; Jones, Timothy A; Jones, Sherri M; Pyott, Sonja J.

In: Hearing Research, Vol. 321, 01.03.2015, p. 52-64.

Research output: Contribution to journalArticle

@article{c2189f0beaa948aca9ab0480d46d00b6,
title = "Deletion of Shank1 has minimal effects on the molecular composition and function of glutamatergic afferent postsynapses in the mouse inner ear",
abstract = "Shank proteins (1-3) are considered the master organizers of glutamatergic postsynaptic densities in the central nervous system, and the genetic deletion of either Shank1, 2, or 3 results in altered composition, form, and strength of glutamatergic postsynapses. To investigate the contribution of Shank proteins to glutamatergic afferent synapses of the inner ear and especially cochlea, we used immunofluorescence and quantitative real time PCR to determine the expression of Shank1, 2, and 3 in the cochlea. Because we found evidence for expression of Shank1 but not 2 and 3, we investigated the morphology, composition, and function of afferent postsynaptic densities from defined tonotopic regions in the cochlea of Shank1-/- mice. Using immunofluorescence, we identified subtle changes in the morphology and composition (but not number and localization) of cochlear afferent postsynaptic densities at the lower frequency region (8kHz) in Shank1-/- mice compared to Shank1+/+ littermates. However, we detected no differences in auditory brainstem responses at matching or higher frequencies. We also identified Shank1 in the vestibular afferent postsynaptic densities, but detected no differences in vestibular sensory evoked potentials in Shank1-/- mice compared to Shank1+/+ littermates. This work suggests that Shank proteins play a different role in the development and maintenance of glutamatergic afferent synapses in the inner ear compared to the central nervous system.",
keywords = "ABR, AMPAR, CNS, CTBP2, DIC, GKAP, IHC, PSD, VsEPs",
author = "Braude, {Jeremy P.} and Sarath Vijayakumar and Katherine Baumgarner and Rebecca Laurine and Jones, {Timothy A} and Jones, {Sherri M} and Pyott, {Sonja J.}",
year = "2015",
month = "3",
day = "1",
doi = "10.1016/j.heares.2015.01.008",
language = "English (US)",
volume = "321",
pages = "52--64",
journal = "Hearing Research",
issn = "0378-5955",
publisher = "Elsevier",

}

TY - JOUR

T1 - Deletion of Shank1 has minimal effects on the molecular composition and function of glutamatergic afferent postsynapses in the mouse inner ear

AU - Braude, Jeremy P.

AU - Vijayakumar, Sarath

AU - Baumgarner, Katherine

AU - Laurine, Rebecca

AU - Jones, Timothy A

AU - Jones, Sherri M

AU - Pyott, Sonja J.

PY - 2015/3/1

Y1 - 2015/3/1

N2 - Shank proteins (1-3) are considered the master organizers of glutamatergic postsynaptic densities in the central nervous system, and the genetic deletion of either Shank1, 2, or 3 results in altered composition, form, and strength of glutamatergic postsynapses. To investigate the contribution of Shank proteins to glutamatergic afferent synapses of the inner ear and especially cochlea, we used immunofluorescence and quantitative real time PCR to determine the expression of Shank1, 2, and 3 in the cochlea. Because we found evidence for expression of Shank1 but not 2 and 3, we investigated the morphology, composition, and function of afferent postsynaptic densities from defined tonotopic regions in the cochlea of Shank1-/- mice. Using immunofluorescence, we identified subtle changes in the morphology and composition (but not number and localization) of cochlear afferent postsynaptic densities at the lower frequency region (8kHz) in Shank1-/- mice compared to Shank1+/+ littermates. However, we detected no differences in auditory brainstem responses at matching or higher frequencies. We also identified Shank1 in the vestibular afferent postsynaptic densities, but detected no differences in vestibular sensory evoked potentials in Shank1-/- mice compared to Shank1+/+ littermates. This work suggests that Shank proteins play a different role in the development and maintenance of glutamatergic afferent synapses in the inner ear compared to the central nervous system.

AB - Shank proteins (1-3) are considered the master organizers of glutamatergic postsynaptic densities in the central nervous system, and the genetic deletion of either Shank1, 2, or 3 results in altered composition, form, and strength of glutamatergic postsynapses. To investigate the contribution of Shank proteins to glutamatergic afferent synapses of the inner ear and especially cochlea, we used immunofluorescence and quantitative real time PCR to determine the expression of Shank1, 2, and 3 in the cochlea. Because we found evidence for expression of Shank1 but not 2 and 3, we investigated the morphology, composition, and function of afferent postsynaptic densities from defined tonotopic regions in the cochlea of Shank1-/- mice. Using immunofluorescence, we identified subtle changes in the morphology and composition (but not number and localization) of cochlear afferent postsynaptic densities at the lower frequency region (8kHz) in Shank1-/- mice compared to Shank1+/+ littermates. However, we detected no differences in auditory brainstem responses at matching or higher frequencies. We also identified Shank1 in the vestibular afferent postsynaptic densities, but detected no differences in vestibular sensory evoked potentials in Shank1-/- mice compared to Shank1+/+ littermates. This work suggests that Shank proteins play a different role in the development and maintenance of glutamatergic afferent synapses in the inner ear compared to the central nervous system.

KW - ABR

KW - AMPAR

KW - CNS

KW - CTBP2

KW - DIC

KW - GKAP

KW - IHC

KW - PSD

KW - VsEPs

UR - http://www.scopus.com/inward/record.url?scp=84922356094&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84922356094&partnerID=8YFLogxK

U2 - 10.1016/j.heares.2015.01.008

DO - 10.1016/j.heares.2015.01.008

M3 - Article

VL - 321

SP - 52

EP - 64

JO - Hearing Research

JF - Hearing Research

SN - 0378-5955

ER -