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Electrical feedback in the cone pedicle: a computational analysis.
Andrey V Dmitriev1, Stuart C Mangel
1Dept. of Neuroscience, The Ohio State University College of Medicine, 333 W. 10th Ave., Columbus, OH 43210, USA. dmitriev.4@osu.edu
Journal of Neurophysiology
|December 2, 2005
Summary
Electrical feedback from retinal horizontal cells to cones is unlikely. Calculations suggest this mechanism is inefficient and contradicts experimental data, indicating negative feedback is likely chemical, not electrical.
Area of Science:
- Neuroscience
- Retinal Physiology
Background:
- Neurons typically require gap junctions for direct electrical interaction.
- A proposed electrical mechanism involving cone synaptic terminals and horizontal cells could explain negative feedback.
- Recent findings on horizontal cell hemichannels renewed interest in electrical feedback.
Purpose of the Study:
- To quantitatively evaluate the role of hemichannels and glutamate channels in electrical feedback from horizontal cells to cones.
- To determine if electrical feedback mechanisms are functionally significant in the retina.
Main Methods:
- Quantitative evaluation and computational modeling of electrical feedback pathways.
- Analysis of resistance parameters in the retinal extracellular space and horizontal cell membranes.
- Comparison of model predictions with experimental data under different light conditions.
Main Results:
- Calculations indicate that electrical feedback effectiveness is very low due to necessary resistance limitations for synaptic transmission.
- Electrical feedback is predicted to be stronger in the dark, contradicting experimental observations of light adaptation.
- The proposed electrical negative feedback model implies a stronger, unreported electrical positive feedback.
Conclusions:
- Electrical feedback from horizontal cells to cones is unlikely to play a significant functional role.
- The observed negative feedback is more likely mediated by a chemical mechanism.
- This study refutes electrical hypotheses and supports chemical signaling in retinal feedback loops.