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J Neurosci. 2014 Apr 30;34(18):6128-39. doi: 10.1523/JNEUROSCI.4941-13.2014.

Kainate receptors mediate signaling in both transient and sustained OFF bipolar cell pathways in mouse retina.

Author information

  • 1Department of Ophthalmology and Visual Science, Department of Cellular and Molecular Physiology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, Connecticut 06511, Department of Anatomical Sciences and Neurobiology, University of Louisville, School of Medicine, Louisville, Kentucky 40202, and Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, Virginia 20147.

Abstract

A fundamental question in sensory neuroscience is how parallel processing is implemented at the level of molecular and circuit mechanisms. In the retina, it has been proposed that distinct OFF cone bipolar cell types generate fast/transient and slow/sustained pathways by the differential expression of AMPA- and kainate-type glutamate receptors, respectively. However, the functional significance of these receptors in the intact circuit during light stimulation remains unclear. Here, we measured glutamate release from mouse bipolar cells by two-photon imaging of a glutamate sensor (iGluSnFR) expressed on postsynaptic amacrine and ganglion cell dendrites. In both transient and sustained OFF layers, cone-driven glutamate release from bipolar cells was blocked by antagonists to kainate receptors but not AMPA receptors. Electrophysiological recordings from bipolar and ganglion cells confirmed the essential role of kainate receptors for signaling in both transient and sustained OFF pathways. Kainate receptors mediated responses to contrast modulation up to 20 Hz. Light-evoked responses in all mouse OFF bipolar pathways depend on kainate, not AMPA, receptors.

KEYWORDS:

OFF bipolar cell; glutamate sensor; kainate receptor; mouse; retinal circuitry; two-photon imaging

PMID:
24790183
[PubMed - indexed for MEDLINE]
PMCID:
PMC4004803
Free PMC Article
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