Research article summary (published 14 Sep 2009):

Negative shift in the glycine reversal potential mediated by a Ca2+- and pH-dependent mechanism in interneurons.

Full Abstract

Cartwheel cells are glycinergic auditory interneurons which fire Na(+)- and Ca(2+)-dependent spike bursts, termed complex spikes, and which synapse on both principal cells and one another. The reversal potential for glycine (E(gly)) can be hyperpolarizing or depolarizing in cartwheel cells, and many cells are even excited by glycine. We explored the role of spike activity in determining E(gly) in mouse cartwheel cells using gramicidin perforated-patch recording. E(gly) was found to shift toward more negative potentials after a period of complex spiking or Ca(2+) spiking induced by depolarization, thus enhancing glycine's inhibitory effect for approximately 30 s following cessation of spiking. Combined perforated patch electrophysiology and imaging studies showed that the negative E(gly) shift was triggered by a Ca(2+)-dependent intracellular acidification. The effect on E(gly) was likely caused by bicarbonate-Cl(-) exchanger-mediated reduction in intracellular Cl(-), as H(2)DIDS and removal of HCO(3)(-)/CO(2) inhibited the negative E(gly) shift. The outward Cl(-) flux underlying the negative shift in E(gly) opposed a positive shift triggered by passive Cl(-) redistribution during the depolarization. Thus, a Ca(2+)-dependent mechanism serves to maintain or enhance the strength of inhibition in the face of increased excitatory activity.

Author information

Author/s: Kim, Yuil (Y); Trussell, Laurence O (LO);

Affiliation: Neuroscience Graduate Program, Oregon Health & Science University, Portland, Oregon 97239, USA.

Grants: R37NS28901 (Agency:NINDS NIH HHS)

Journal and publication information

Publication Type: In Vitro; Journal Article; Research Support, N.I.H., Extramural

Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience (J Neurosci), published in United States. (Language: eng)

Reference: 2009-Sep; vol 29 (issue 37) : pp 11495-510

Dates: Created 2009/09/17; Completed 2009/10/02;

PMID: 19759298, status: MEDLINE (last retrieval date: 10/2/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Action Potentials - drug effects; physiology Animals Animals, Newborn Benzopyrans - metabolism Bicarbonates - metabolism Biophysics Calcium - metabolism Chlorides - metabolism Cochlear Nucleus - cytology Dose-Response Relationship, Drug Electric Stimulation - methods Excitatory Amino Acid Antagonists - pharmacology Glycine - pharmacology Glycine Agents - pharmacology

Glycine Agents - pharmacology HEPES - pharmacology Hydrogen-Ion Concentration Interneurons - drug effects Mice Mice, Inbred ICR Models, Biological Patch-Clamp Techniques - methods Quinoxalines - pharmacology Sodium Channel Blockers - pharmacology Sodium-Bicarbonate Symporters - metabolism Tetrodotoxin - pharmacology Time Factors gamma-Aminobutyric Acid - pharmacology

Associated Chemicals: Benzopyrans (0) ; Bicarbonates (0) ; Chlorides (0) ; Excitatory Amino Acid Antagonists (0) ; Glycine Agents (0) ; Quinoxalines (0) ; SNARF dye (0) ; Sodium Channel Blockers (0) ; Sodium-Bicarbonate Symporters (0) ; FG 9041 (2379-57-9) ; Tetrodotoxin (4368-28-9) ; gamma-Aminobutyric Acid (56-12-2) ; Glycine (56-40-6) ; HEPES (7365-45-9) ; Calcium (7440-70-2)

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