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Potassium‐Dependent Coupling of Retinal Astrocyte Light Response to Müller Glia
Author(s) -
Holden Joseph Matthew,
Boal Andrew M.,
Wareham Lauren Katie,
Calkins David John
Publication year - 2025
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.70022
Subject(s) - biology , neuroscience , retina , depolarization , astrocyte , muller glia , retinal , premovement neuronal activity , stimulus (psychology) , soma , neuroglia , neuron , electrophysiology , biophysics , central nervous system , microbiology and biotechnology , biochemistry , stem cell , psychology , progenitor cell , psychotherapist
ABSTRACT Astrocytes throughout the central nervous system mediate a variety of functions to support proper tissue physiology, including the regulation of blood flow and providing metabolic support to neurons. There is also growing appreciation for their role in directly modulating neuronal excitability and information transfer. Recently, we reported that astrocytes in the retina exhibit an array of neuronal‐associated microstructural motifs whose structure and placement suggest roles in monitoring neuronal electrical activity or direct modulation of excitability. In this study, we record whole‐cell patch clamp responses of astrocytes in intact retina to both light and voltage step as a precursor to studying the detailed physiology of individual microstructural motifs. Retinal astrocytes exhibit small amplitude, graded depolarization to both light ON and OFF stimuli with waveforms that closely resemble those of Müller glial endfeet, from which we also recorded. Depolarization is due to potassium influx, with the major source likely being focal release from Müller endfeet onto astrocyte soma. Both macroglia additionally share current–voltage relationships and exhibit stimulus‐dependent changes in ionic permeability. The results suggest a pathway of communication from Müller cells to astrocytes that could support broader retinal modulation beyond potassium spatial buffering.
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