Journal
JOURNAL OF NEUROSCIENCE
Volume 26, Issue 6, Pages 1759-1766Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3895-05.2006
Keywords
retina; ryanodine receptors; calcium channels; glutamate; synaptic transmission; rod
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Funding
- PHS HHS [NEI-05725] Funding Source: Medline
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Retinal rod photoreceptors are depolarized in darkness to approximately -40 mV, a state in which they maintain sustained glutamate release despite low levels of calcium channel activation. Blocking voltage-gated calcium channels or ryanodine receptors (RyRs) at the rod presynaptic terminal suppressed synaptic communication to bipolar cells. Spontaneous synaptic events were also inhibited when either of these pathways was blocked. This indicates that both calcium influx and calcium release from internal stores are required for the normal release of transmitter of the rod. RyR-independent release can be evoked by depolarization of a rod to a supraphysiological potential (-20 mV) that activates a large fraction of voltage-gated channels. However, this calcium channel-mediated release depletes rapidly if RyRs are blocked, indicating that RyRs support prolonged glutamate release. Thus, the rod synapse couples a small transmembrane calcium influx with a RyR-dependent amplification mechanism to support continuous vesicle release.
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