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The Journal of Neuroscience, February 8, 2006, 26(6):1759-1766; doi:10.1523/JNEUROSCI.3895-05.2006

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Cellular/Molecular
Synaptic Transmission Mediated by Internal Calcium Stores in Rod Photoreceptors

Anuradha Suryanarayanan and Malcolm M. Slaughter

Department of Physiology and Biophysics, University at Buffalo, Buffalo, New York 14214

Correspondence should be addressed to Malcolm M. Slaughter, Department of Physiology and Biophysics, University at Buffalo, 124 Sherman Hall, Buffalo, NY 14214. Email: mslaught{at}buffalo.edu

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.

Key words: retina; ryanodine receptors; calcium channels; glutamate; synaptic transmission; rod

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Received Sept. 14, 2005; revised Dec. 27, 2005; accepted Dec. 28, 2005.

Correspondence should be addressed to Malcolm M. Slaughter, Department of Physiology and Biophysics, University at Buffalo, 124 Sherman Hall, Buffalo, NY 14214. Email: mslaught{at}buffalo.edu

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