Synaptically localized calcium channels shape the timecourse of
synaptic release, are a prominent site for neuromodulation, and have
been implicated in genetic disease. In retina, it is well established
that L-type calcium channels play a major role in mediating release of
glutamate from the photoreceptors and bipolar cells. However, little is
known about which calcium channels are coupled to synaptic exocytosis
of glycine, which is primarily released by amacrine cells. A recent
report indicates that glycine release from spiking AII amacrine cells
relies exclusively upon L-type calcium channels. To identify calcium
channel types controlling neurotransmitter release from the population
of glycinergic neurons that drive retinal ganglion cells, we recorded
electrical and potassium evoked inhibitory synaptic currents (IPSCs)
from these postsynaptic neurons in retinal slices from tiger
salamanders. The L-channel antagonist nifedipine strongly inhibited
release and FPL64176, an L-channel agonist, greatly enhanced it,
indicating a significant role for L-channels. ω-Conotoxin MVIIC,
an N/P/Q-channel antagonist, strongly inhibited release,
indicating an important role for non-L channels. While the
P/Q-channel blocker ω-Aga IVA produced only small effects, the
N-channel blocker ω-conotoxin GVIA strongly inhibited release.
Hence, N-type and L-type calcium channels appear to play major roles,
overall, in mediating synaptic release of glycine onto retinal ganglion
cells.