Abstract
Purpose: :
In retinal photoreceptors, light adaptation has long been defined as the physiological changes that occur in the presence of steady background light. Recently, however, a long–lasting form of light–adaptation termed "adaptive acceleration" has been found to speed response recovery for many tens of seconds following the offset of saturating light. Here, we investigated the requirements for induction and maintenance of adaptive acceleration in order to gain insight into the responsible mechanism.
Methods: :
Suction electrodes were used to record the outer segment membrane current of individual rods of wild type mice before, during, and after and adapting stimulus (500 nm light) that varied both in intensity and duration. Adaptive acceleration was probed using brief (10 ms) flashes of light of fixed intensity.
Results: :
As described previously, adaptive acceleration was easily induced using an adapting stimulus that bleached 3% of rhodopsin over a time period of 3 minutes. However, the equivalent bleach over a much shorter time period (1–3 seconds) failed to induce significant response acceleration. As the duration of the adapting stimulus was increased, the magnitude of the acceleration increased in a manner that could be fitted by a single exponential function with a time constant of 35 s. Recordings of the membrane current in darkness before and after the induction of adaptive acceleration showed that the speeding of response recovery was not associated with a detectable change in the cellular dark noise variance.
Conclusions: :
These results indicate that the induction of adaptive acceleration requires cascade activity that persists for at least 30 seconds. The lack of an effect of the adapting stimulus on cellular dark noise rules out lingering activity of rhodopsin and PDE as the source of the persistent response acceleration.
Keywords: photoreceptors • electrophysiology: non-clinical • signal transduction