A cGMP-gated current can control exocytosis at cone synapses
1Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637.
Neuron
|October 1, 1994
Summary
Calcium influx via voltage-gated and cGMP-gated channels triggers exocytosis in retinal photoreceptors. The cGMP-gated current ensures sustained transmitter release across the full physiological voltage range.
Area of Science:
- Neuroscience
- Photoreceptor Physiology
- Cellular Biology
Background:
- Voltage-gated Ca2+ currents in cone photoreceptors are limited in their physiological voltage range.
- This limited range suggests insufficient capacity for controlling transmitter release.
- Understanding calcium influx mechanisms is crucial for photoreceptor function.
Purpose of the Study:
- To investigate the mechanisms of calcium influx and exocytosis in cone and rod photoreceptors.
- To determine the role of different calcium channels in initiating and sustaining exocytosis.
- To assess the sufficiency of voltage-gated calcium currents in controlling transmitter release.
Main Methods:
- Whole-cell voltage clamp recordings from solitary salamander cone and rod photoreceptors.
- Measurement of membrane current and capacitance changes associated with exocytosis.
- Analysis of calcium influx through voltage-gated and cGMP-gated channels.
Main Results:
- Calcium influx through voltage-gated Ca2+ channels initiated exocytosis in both photoreceptor types.
- Calcium influx via a cGMP-gated channel in cones also initiated exocytosis.
- The cGMP-gated current sustained exocytosis throughout the entire physiological voltage range.
Conclusions:
- Both voltage-gated and cGMP-gated calcium channels play a role in initiating exocytosis in photoreceptors.
- cGMP-gated channels provide a sustained calcium influx necessary for transmitter release over the full physiological voltage range in cones.
- These findings reveal a more comprehensive mechanism for regulating transmitter release in photoreceptors.
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