Excitatory modulation in the cochlear nucleus through group I metabotropic glutamate receptor activation.

J Neurosci

Department of Biological Sciences, University at Buffalo, State University of New York, Buffalo, New York 14260, USA.

Published: May 2011

AI Article Synopsis

  • Activation of group I metabotropic glutamate receptors (mGluRs) influences the development and physiological responses of bushy cells in the auditory system, particularly in the anteroventral cochlear nucleus (AVCN).
  • Activation of mGluRs leads to depolarization of these cells, increases their firing probability in response to auditory nerve stimulation, and reduces response latency and jitter, suggesting enhanced auditory processing.
  • The interaction between mGluRs and presynaptic GABA(B) receptors provides a mechanism for balancing excitatory and inhibitory signals, allowing for refined auditory signal relay.

Article Abstract

Activation of group I metabotropic glutamate receptors (mGluRs) has been suggested to modulate development of auditory neurons. However, the acute effects of mGluR activation on physiological response properties are unclear. To address this, we studied the effects of mGluRs in bushy cells (BCs) of the mammalian anteroventral cochlear nucleus (AVCN). Activation of mGluRs with dihydroxyphenylglycine (DHPG) caused depolarization of BCs in mice as old as P42, but did not affect neurotransmitter release by presynaptic auditory nerve (AN) fibers. Application of mGluR antagonists indicated that mGluRs are tonically active, and are highly sensitive to small elevations in ambient glutamate by the glutamate reuptake blocker threo-β-benzyloxyaspartic acid (TBOA). mGluR-mediated depolarization enhanced the firing probability in response to AN stimulation, and reduced the latency and jitter. Furthermore, excitation through postsynaptic mGluRs can significantly counterbalance the inhibitory effects of presynaptic GABA(B) receptors. Thus, interaction between these two modulatory pathways may provide additional flexibility for fine-tuning the BC relay.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104504PMC
http://dx.doi.org/10.1523/JNEUROSCI.1193-11.2011DOI Listing

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