Endogenous mGluR activity suppresses GABAergic transmission in avian cochlear nucleus magnocellularis neurons.
GABAergic transmission in the avian cochlear nucleus magnocellularis (NM) of the chick is subject to modulation by gamma-aminobutyric acid type B (GABA(B)) autoreceptors. Here, I investigated modulation of GABAergic transmission in NM by metabotropic glutamate receptors (mGluRs) with whole cell recordings in brain slice preparations. I found that tACPD, a nonspecific mGluR agonist, exerted dose-dependent suppression on evoked inhibitory postsynaptic currents (eIPSCs) in NM neurons. At concentrations of 100 or 200 microM, tACPD increased the failure rate of GABAergic transmission. Agonists for group I (3,5-DHPG, 200 microM), group II (DCG-IV, 2 microM), and group III (L-AP4, 10 microM) mGluRs produced a significant reduction in the amplitude of eIPSCs and a significant increase in failure rate, indicating the involvement of multiple mGluRs in this modulation. The frequency, but not the amplitude, of miniature IPSCs (mIPSCs) was decreased significantly by 3,5-DHPG or DCG-IV. Neither frequency nor amplitude of mIPSCs was affected by L-AP4. mGluR antagonists LY341495 (20 microM) plus CPPG (10 microM) significantly increased the amplitude of eIPSCs, indicating that endogenous mGluR activity suppresses GABA release to NM neurons. Furthermore, blockage of mGluRs increased GABA-evoked discharges recorded under physiological Cl(-) concentrations, whereas tACPD (100 microM) eliminated them. The results indicate that mGluRs play important roles in achieving balanced excitation and inhibition in NM and preserving fidelity of temporal information encoded by NM neurons.
Lu
Yong
Y
Department of Neurobiology, Northeastern Ohio Universities College of Medicine, 4209 State Route 44, Rootstown, OH 44272, USA. ylu@neoucom.edu
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D002645:Chickens / Q000502:physiology*; D017626:Cochlear Nucleus / Q000166:cytology* / Q000502:physiology*; D004558:Electric Stimulation; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D058786:GABA-B Receptor Agonists; D058788:GABA-B Receptor Antagonists; D005998:Glycine / Q000031:analogs & derivatives / Q000494:pharmacology; D066298:In Vitro Techniques; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D008959:Models, Neurological; D009474:Neurons / Q000502:physiology*; D018408:Patch-Clamp Techniques; D018080:Receptors, GABA-B / Q000502:physiology; D018094:Receptors, Metabotropic Glutamate / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000502:physiology; D012118:Resorcinols / Q000494:pharmacology; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*; D014966:Xanthenes / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D000596:Amino Acids; D018691:Excitatory Amino Acid Antagonists; D058786:GABA-B Receptor Agonists; D058788:GABA-B Receptor Antagonists; C114624:LY 341495; D018080:Receptors, GABA-B; D018094:Receptors, Metabotropic Glutamate; D012118:Resorcinols; D014966:Xanthenes; D005680:gamma-Aminobutyric Acid; C079215:3,5-dihydroxyphenylglycine; D015763:2-Amino-5-phosphonovalerate; D005998:Glycine