Abstract
Purpose: :
The transition between light adapted and dark adapted conditions is associated with a profound functional reorganization of the vertebrate retina. Retinal dopamine receptors are known to activate mechanisms that optimize retinal signal transfer under conditions of light adaptation. In this study, we have used brimonidine, a selective alpha-2 adrenergic receptor agonist, to determine whether alpha-2 receptors regulate retinal mechanisms associated with dark adaptation.
Methods: :
Simultaneous recordings of the electroretinogram (ERG) and spiking activity of single retinal ganglion cells (RGCs) were obtained, using conventional methods, from a dark-adapted ex-vivo rabbit retina preparation. Dim diffuse light stimuli were used to elicit ERG b-wave responses. RGC responses to the same stimuli were characterized as either "ON" or "OFF" type. Test agents were bath applied via the perfusion medium.
Results: :
Application of dopamine (10 - 20 µM) was associated with reduced amplitude and decreased time-to-peak of the b-wave, reduction of both ON and OFF RGC responses (spike density), and an increased latency of RGC ON responses. Application of brimonidine (100 - 150 nM) was associated with an increase in both the amplitude and time-to-peak of the b-wave, an increase in the amplitude of ON RGC responses, and an increase in the latency of OFF RGC responses. The different effects of dopamine and brimonidine on the ERG b-wave and either ON or OFF RGC responses is consistent with the opposite actions of alpha-2 receptors and dopamine type D1 receptors to either decrease or increase, respectively, the intracellular levels of cAMP.
Conclusions: :
These results suggest that retinal light/dark adaptation reflects the balance of activation of alpha-2 receptors and type D1 dopamine receptors and that these two pathways act in concert to regulate the functional organization of the retina under different conditions of ambient illumination.
Keywords: electrophysiology: non-clinical • neurotransmitters/neurotransmitter systems • ganglion cells