Synaptic Transmission Mediated by Internal Calcium Stores in Rod Photoreceptors

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 suppresse...

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Bibliographic Details
Published in:The Journal of neuroscience 2006-02, Vol.26 (6), p.1759-1766
Main Authors: Suryanarayanan, Anuradha, Slaughter, Malcolm M
Format: Article
Language:English
Subjects:
Ambystoma
Animals
Calcium Channel Blockers - pharmacology
Calcium Signaling - physiology
Electrophysiology
In Vitro Techniques
Membrane Potentials - physiology
Photoreceptor Cells - physiology
Retinal Rod Photoreceptor Cells - physiology
Ryanodine - pharmacology
Ryanodine Receptor Calcium Release Channel - drug effects
Ryanodine Receptor Calcium Release Channel - physiology
Synapses - drug effects
Synapses - physiology
Synaptic Transmission - physiology
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Summary: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.
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.3895-05.2006