Mechanisms of temporal filtering at the bipolar cell terminal.
A, A schematic diagram is shown of a bipolar cell axon with large and small synaptic terminals, synapsing on amacrine and ganglion cells. B, A close-up view of the large terminal (dashed square in A) shows some mechanisms that influence temporal filtering. When the electrical signal enters the terminal, it is transformed by the low-pass filter, shown as the circuit diagram, formed by axial resistance, membrane resistance, and capacitance. In some bipolar cells, voltage-gated sodium channels generate spikes at the terminal [28]. Depolarization opens voltage-gated calcium channels, and the influx of calcium ions activates vesicle fusion and neurotransmitter release, signaling to amacrine and ganglion cells through glutamate receptors. Vesicle cycling is described mathematically based on kinetic measurements by an activation rate constant (rA) and the recovery rates (rR1, rR2, rR3). The rate constant rR1 is related to the rate of endocytosis, and rR2 and rR3 correspond to the rate of refilling of two “pools” of vesicles known as the recycling pool and the readily releasable pool (RRP), respectively [25]. Intracellular calcium ions diffuse from calcium channels to calcium-gated potassium and chloride channels, which produce a delayed hyperpolarization, attenuating steady inputs and contributing to a biphasic band-pass filter. Finally, GABAergic or glycinergic inhibitory amacrine cells have pre- and post-synaptic control over signal transmission, also contributing to a biphasic filter.
