Open AccessA group I metabotropic glutamate receptor controls synaptic gain between rods and rod bipolar cells in the mouse retina
Author(s) -
Hellmer Chase B.,
Clemons Melissa Rampino,
Nawy Scott,
Ichinose Tomomi
Publication year - 2018
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13885
Subject(s) - metabotropic glutamate receptor 1 , metabotropic glutamate receptor , metabotropic glutamate receptor 6 , metabotropic glutamate receptor 5 , microbiology and biotechnology , protein kinase c , biology , metabotropic receptor , long term potentiation , biophysics , chemistry , glutamate receptor , neuroscience , signal transduction , biochemistry , receptor
The canonical mG luR6‐Trpm1 pathway that generates the sign‐inverting signal between photoreceptors and ON bipolar cells has been well described. However, one type of ON bipolar cell, the rod bipolar cell ( RBC ), additionally is thought to express the group I mG luRs whose function is unknown. We examined the role of group I mG luRs in mouse RBC s and here provide evidence that it controls synaptic gain between rods and RBC s. In dark‐adapted conditions, the mG luR1 antagonists LY 367385 and (RS)‐1‐Aminoindan‐1,5‐dicarboxylic acid, but not the mG luR5 antagonist 2‐Methyl‐6‐(phenylethynyl)pyridine hydrochloride reduced the light‐evoked responses in RBC s indicating that mG luR1, but not mG luR5, serves to potentiate RBC responses. Perturbing the downstream phospholipase C ( PLC )‐protein kinase C ( PKC ) pathway by inhibiting PLC , tightly buffering intracellular Ca 2+ , or preventing its release from intracellular stores reduced the synaptic potentiation by mG luR1. The effect of mG luR1 activation was dependent upon adaptation state, strongly increasing the synaptic gain in dark‐, but not in light‐adapted retinas, or in the presence of a moderate background light, consistent with the idea that mG luR1 activation requires light‐dependent glutamate release from rods. Moreover, immunostaining revealed that protein kinase C α (PKC α ) is more strongly expressed in RBC dendrites in dark‐adapted conditions, revealing an additional mechanism behind the loss of mG luR1 potentiation. In light‐adapted conditions, exogenous activation of mG luR1 with the agonist 3,5‐Dihydroxyphenylglycine increased the mG luR6 currents in some RBC s and decreased it in others, suggesting an additional action of mG luR1 that is unmasked in the light‐adapted state. Elevating intracellular free Ca 2+ , consistently resulted in a decrease in synaptic gain. Our results provide evidence that mG luR1 controls the synaptic gain in RBCs.