Abstract
Rod photoreceptors generate amplified, reproducible responses to single photons via a G protein signaling cascade. Surprisingly, genetic perturbations that dramatically alter the deactivation of the principal signal amplifier, the GPCR rhodopsin (R&z.ast;), do not much alter the amplitude of single-photon responses (SPRs). These same perturbations, when crossed into a line lacking calcium feedback regulation of cGMP synthesis, produced much larger alterations in SPR amplitudes. Analysis of SPRs from rods with and without feedback reveal that the consequences of trial-to-trial fluctuations in R&z.ast; lifetime in normal rods are also dampened by feedback regulation of cGMP synthesis. Thus, calcium feedback trumps the mechanisms of R&z.ast; deactivation in determining the SPR amplitude, attenuating responses arising from longer R&z.ast; lifetimes to a greater extent than those arising from shorter ones. As a result, rod SPRs achieve a more stereotyped amplitude, a characteristic considered important for reliable transmission through the visual system.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 370-382 |
| Number of pages | 13 |
| Journal | Neuron |
| Volume | 76 |
| Issue number | 2 |
| DOIs | |
| State | Published - Oct 18 2012 |
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ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Calcium Feedback to cGMP Synthesis Strongly Attenuates Single-Photon Responses Driven by Long Rhodopsin Lifetimes. / Gross, Owen P.; Pugh Jr, Edward N; Burns, Marie E.
In: Neuron, Vol. 76, No. 2, 18.10.2012, p. 370-382.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Calcium Feedback to cGMP Synthesis Strongly Attenuates Single-Photon Responses Driven by Long Rhodopsin Lifetimes
AU - Gross, Owen P.
AU - Pugh Jr, Edward N
AU - Burns, Marie E
PY - 2012/10/18
Y1 - 2012/10/18
N2 - Rod photoreceptors generate amplified, reproducible responses to single photons via a G protein signaling cascade. Surprisingly, genetic perturbations that dramatically alter the deactivation of the principal signal amplifier, the GPCR rhodopsin (R&z.ast;), do not much alter the amplitude of single-photon responses (SPRs). These same perturbations, when crossed into a line lacking calcium feedback regulation of cGMP synthesis, produced much larger alterations in SPR amplitudes. Analysis of SPRs from rods with and without feedback reveal that the consequences of trial-to-trial fluctuations in R&z.ast; lifetime in normal rods are also dampened by feedback regulation of cGMP synthesis. Thus, calcium feedback trumps the mechanisms of R&z.ast; deactivation in determining the SPR amplitude, attenuating responses arising from longer R&z.ast; lifetimes to a greater extent than those arising from shorter ones. As a result, rod SPRs achieve a more stereotyped amplitude, a characteristic considered important for reliable transmission through the visual system.
AB - Rod photoreceptors generate amplified, reproducible responses to single photons via a G protein signaling cascade. Surprisingly, genetic perturbations that dramatically alter the deactivation of the principal signal amplifier, the GPCR rhodopsin (R&z.ast;), do not much alter the amplitude of single-photon responses (SPRs). These same perturbations, when crossed into a line lacking calcium feedback regulation of cGMP synthesis, produced much larger alterations in SPR amplitudes. Analysis of SPRs from rods with and without feedback reveal that the consequences of trial-to-trial fluctuations in R&z.ast; lifetime in normal rods are also dampened by feedback regulation of cGMP synthesis. Thus, calcium feedback trumps the mechanisms of R&z.ast; deactivation in determining the SPR amplitude, attenuating responses arising from longer R&z.ast; lifetimes to a greater extent than those arising from shorter ones. As a result, rod SPRs achieve a more stereotyped amplitude, a characteristic considered important for reliable transmission through the visual system.
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UR - http://www.scopus.com/inward/citedby.url?scp=84867725368&partnerID=8YFLogxK
U2 - 10.1016/j.neuron.2012.07.029
DO - 10.1016/j.neuron.2012.07.029
M3 - Article
C2 - 23083739
AN - SCOPUS:84867725368
VL - 76
SP - 370
EP - 382
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 2
ER -