Cochlear dopamine release is modulated by group II metabotropic glutamate receptors via GABAergic neurotransmission
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Acknowledgements
The authors thank Erika Tischler for her technical contributions. This work was supported in part by the Hungarian Research Fund (OTKA T 034622, T 037459 and Ts 040736), the Hungarian Medical Research Foundation (470/2003; 123/2003) and the European Commission FP6 Integrated Project EUROHEAR, LSHG-CT-20054-512063.
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2022, Hearing ResearchCitation Excerpt :mGluR1 has been implicated in enhancing the acetylcholine (ACh)-induced inhibition of IHCs by the transient medial olivocochlear (MOC) efferent innervation that occurs prior to hearing onset (see below), suggesting that it may also affect maturation of the ascending auditory pathway (Ye et al., 2017). Non-specific group II (mGluR2 and 3) agonists have been reported to increase dopamine release in the guinea pig cochlea via a disinhibitory mechanism in which glutamate activates mGluR2 on GABAergic, but not dopaminergic, lateral olivocochlear (LOC) efferent terminals, inhibiting tonic GABA release and thus disinhibiting dopamine release (Doleviczényi et al., 2005). This would suggest a role for mGluR2 in self-regulation of glutamate signaling via an increase in inhibitory dopamine signaling through the LOC system.
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2014, NeuroscienceCitation Excerpt :Modulation rather than mediation of synaptic transmission by group II mGluRs has been reported in the cochlea. In vitro microvolume superfusion on guinea pig cochlea preparations shows that pharmacological activation of group II mGluRs, but not group I and III mGluRs, increases dopamine release at the dopaminergic synapses of the lateral olivocochlear system (Doleviczényi et al., 2005). Increased dopamine can activate D2 receptors on IHC afferents, and may lead to protective effects against excitotoxicity caused by excessive glutamate release from the IHCs in response to noise exposure.
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2014, NeuroscienceCitation Excerpt :Considering the protective actions of cochlear DA, several target sites have appeared as candidates for increasing the endogenous DAergic protection. We have already shown that 5-HT6/7 antagonists (Doleviczényi et al., 2008), group II mGluR ligands (Doleviczényi et al., 2005), selective NMDA receptor agonists (Halmos et al., 2008) and D2 DA receptor antagonists (Halmos et al., 2005) provide new possibilities for the enhancement of DA release from the LOC terminals in the cochlea (Lendvai et al., 2011). Boosting of protective LOC feedback in synchrony with the endogenous, action potential-evoked release of DA seems to be superior to simply evoking DA release from the terminal independently of the on-going axonal activity of the LOC efferents or to directly activating the postsynaptic DA receptors by the administration of appropriate receptor ligands.