In addition to differences in synaptic vesicle pool dynamics, several other mechanisms could contribute to the generation of transient versus sustained responses in parallel ON pathways. One potential factor is the differential expression of glutamate receptor subtypes on the postsynaptic RGCs. Variations in the composition of ionotropic glutamate receptors, such as AMPA and NMDA receptors, can influence the kinetics of excitatory postsynaptic currents and shape the temporal characteristics of the response. Moreover, the presence of metabotropic glutamate receptors (mGluRs) on RGC dendrites could modulate the kinetics of synaptic transmission by regulating intracellular signaling pathways.
Another possible mechanism is the involvement of presynaptic modulatory factors that regulate neurotransmitter release. Neuromodulators, such as dopamine or acetylcholine, can modulate the release of glutamate from bipolar cell terminals and impact the temporal dynamics of synaptic transmission. These neuromodulatory signals can act on presynaptic receptors or intracellular signaling pathways to alter the release probability of synaptic vesicles and influence the kinetics of excitatory inputs to RGCs.
Furthermore, the structural organization of the synaptic machinery at the bipolar cell terminals could play a role in determining the kinetics of glutamate release. Variations in the number and distribution of active zones, the presence of specialized proteins involved in vesicle fusion, or the efficiency of vesicle recycling mechanisms could all contribute to differences in the temporal profile of synaptic transmission between bipolar cell subtypes.