Group i metabotropic glutamate receptors in spiral ganglion neurons contribute to excitatory neurotransmissions in the cochlea
Section snippets
Detection and relative quantification of mGluRIs and G-protein subunits in the cochlea by real-time reverse transcription (RT), polymerase chain reaction (PCR) amplification and cDNA-macroarray
After being anesthetized by ketamine (80 mg/kg; Phoenix Pharmaceutical Inc., St. Joseph, MO, USA) and xylazine (10 mg/kg; Lloyd Laboratories, Shenandoah, IA, USA), mice (strain CD-1) were killed by decapitation. The animal use protocol was approved by the institutional animal use and care committee (IACUC) of the House Ear Institute. All experiments conformed to the international guidelines on the ethical use of animals, and the IACUC ensured that the number of animals used and their suffering
Mgluris and multiple types of g-protein subunits were expressed in the cochlea. immunolabeling showed that a subset of sg neurons expressed mglur1
We first detected the presence of mGluRIs in the cochlea by RT-PCR amplifications. Starting with the same amount of cochlear RNA, mGluR1 and mGluR5 were amplified to a level above the noise floor after about 18 amplification cycles (Fig. 1A). The growth of mGluR5 amplicon lagged significantly behind that of mGluR1. Measured at their respective linear increasing phases on a semi-log scale, as indicated by a horizontal dashed line in Fig. 1, Fig. 4. 9 more PCR cycles were needed for mGluR5 to
Acknowledgements
This study was supported by grants from NIDCD (NIH RO1 04709 and R21 DC04492).
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Diverse identities and sites of action of cochlear neurotransmitters
2022, Hearing ResearchCitation Excerpt :SGNs of guinea pig and rat express mGluR1 (Safieddine and Eybalin, 1995) and a subset show mGluR1 immunolabeling (Peng et al., 2004b). Group I (which includes mGluR1 and mGluR5) agonists induce transient inward currents (Peng et al., 2004b) and evoke action potentials (Kleinlogel et al., 1999; Peng et al., 2004b) in type I SGNs, which can be blocked by mGluR1 antagonists (Kleinlogel et al., 1999). Blocking mGluR1s in vivo had no effect on hearing threshold, but did cause a reduction in both CAP amplitude in response to loud sounds and noise-induced threshold shifts, suggesting that mGluR1 enhances cochlear responses (Peng et al., 2004b).
Cochlear homeostasis: a molecular physiological perspective on maintenance of sound transduction and auditory neurotransmission with noise and ageing
2020, Current Opinion in PhysiologyCitation Excerpt :This complements an earlier in vivo electrophysiological study where DHPG increased spontaneous SGN firing in guinea pig type I afferents adjacent to IHCs, which was blocked by AIDA [89]. Given the evidence that group I mGluR enhance SGN excitability with elevated sound levels, it seems likely that such supplementary drive contributes to cochlear synaptopathy [88]. TRPC3 channels expressed by SGN [36,37] may contribute to SGN glutamatergic excitotoxicity via group I mGluR coupling.
Metabotropic glutamate receptors in auditory processing
2014, NeuroscienceCitation Excerpt :An excitatory action mediated by group I mGluRs in the cochlea has been demonstrated. Application of DHPG, an agonist for group I mGluRs, increases the spike firing of spiral ganglion neurons (Kleinlogel et al., 1999; Oestreicher et al., 2002), accompanied by an increase in intracellular Ca2+ concentration (Peng et al., 2004). In spiral ganglion neurons ACPD, a non-specific mGluR agonist that predominantly activates group I and II mGluRs, produces an inward current under voltage clamp, and causes membrane depolarization and spiking under current clamp (Peng et al., 2004).