Regulation of ON bipolar cell activity

Abstract

Synaptic transmission from photoreceptors to all types of ON bipolar cells is primarily mediated by the mGluR6 receptor. This receptor, which is apparently expressed uniquely in the nervous system by ON bipolar cells, couples negatively to a nonselective cation channel. This arrangement results in a sign reversal at photoreceptor/ON bipolar cell synapse, which is necessary in order to establish parallel ON and OFF pathways in the retina. The synapse is an important target for 2 nd messenger molecules that are known to modulate synaptic transmission elsewhere in the nervous system, 2 nd messengers that act on a time scale ranging from milliseconds to minutes. This review focuses on two of these molecules, Ca 2+ and cGMP, summarizing our current knowledge of how they modulate gain at the photoreceptor/ON bipolar cell synapse, as well as their proposed sites of action within the mGluR6 cascade. The implications of plasticity at this synapse for retinal function will also be examined.

Transient Receptor Potential Melastatin 1 (TRPM1) Is an Ion-conducting Plasma Membrane Channel Inhibited by Zinc Ions

“…In ON-bipolar cells, glutamate released from rod photoreceptor cells activates mGluR6 metabotropic glutamate receptors (16,17). Those receptors in turn activate a poorly understood signaling cascade that involves G␣ o proteins (18,19) and leads to closure of a constitutively active, nonselective cationic conductance (20,21). TRPM1 proteins are necessary for this transduction pathway to work.…”

Expression of α-gustducin in mammalian retinas

“…Retinal ON bipolar cells, including rod bipolar cells, use a G protein-coupled glutamate receptor, mGluR6 [20], and Gao is known to be a representative a subunit of the G protein activated by mGluR6 [21][22][23]. Gb3 and Gg13 are coexpressed in dendrites, somata, and axon terminals of ON bipolar cells, suggesting that Gb3 and Gg13 might selectively participate in signal transduction with other G proteins in ON bipolar cells [14].…”

Glycine receptor alpha subunit (GlyRa) specific inhibition contributes to ganglion cell signaling in mouse retina.

“…In the dark, PRs (rods and cones) constantly release glutamate, which keeps the mGluR6 receptor occupied and inactivates its Gprotein coupled cascade. This keeps the TRPM1 cation channel closed and DBCs relatively hyperpolarized (Koike et al, 2010;Morgans et al, 2009;Snellman et al, 2008). At light onset, PRs reduce glutamate release, which activates the mGluR6 G-protein signaling cascade, opens the TRPM1 cation channel and depolarizes the DBC.…”