Pre- and postsynaptic effects of glutamate in the frog labyrinth
| Autor: | Marta Martini, Gemma Rubbini, Riccardo Fesce, Rita Canella, Maria Lisa Rossi |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Patch-Clamp Techniques GluR and mGluR Glutamic Acid glutamate Pharmacology Neurotransmission Receptors Ionotropic Glutamate Receptors Metabotropic Glutamate NO 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Postsynaptic potential Hair Cells Auditory Animals Glutamate reuptake Hair cell calcium and potassium currents isolated frog labyrinth sensory discharge synaptic transmission Amino Acids 6-Cyano-7-nitroquinoxaline-2 3-dione Aspartic Acid General Neuroscience Glutamate receptor Excitatory Postsynaptic Potentials Glutamic acid 030104 developmental biology Xanthenes chemistry Ear Inner Synapses CNQX Excitatory postsynaptic potential Anura Excitatory Amino Acid Antagonists 030217 neurology & neurosurgery Ionotropic effect |
| Popis: | The role of glutamate in quantal release at the cytoneural junction was examined by measuring mEPSPs and afferent spikes at the posterior canal in the intact frog labyrinth. Release was enhanced by exogenous glutamate, or dl-TBOA, a blocker of glutamate reuptake. Conversely, drugs acting on ionotropic glutamate receptors did not affect release; the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA-R) blocker CNQX decreased mEPSP size in a dose-dependent manner; the NMDA-R blocker d-AP5 at concentrations200 µM did not affect mEPSP size, either in the presence or absence of Mg and glycine. In isolated hair cells, glutamate did not modify Ca currents. Instead, it systematically reduced the compound delayed potassium current, IKD, whereas the metabotropic glutamate receptor (mGluR)-II inverse agonist, (2S)-2-amino-2-[(1S,2S)-2-carboxycycloprop-1-yl]-3-(xanth-9-yl)propanoic acid (LY341495), increased it. Given mGluR-II decrease cAMP production, these finding are consistent with the reported sensitivity of IKD to protein kinase A (PKA)-mediated phosphorylation. LY341495 also enhanced transmitter release, presumably through phosphorylation-mediated facilitation of the release machinery. The observed enhancement of release by glutamate confirms previous literature data, and can be attributed to activation of mGluR-I that promotes Ca release from intracellular stores. Glutamate-induced reduction in the repolarizing IKD may contribute to facilitation of release. Overall, glutamate exerts both a positive feedback action on mGluR-I, through activation of the phospholipase C (PLC)/IP |
| Databáze: | OpenAIRE |
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