Dopaminergic modulation of rod pathway signals does not affect the scotopic ERG of cat at dark-adapted threshold.

1. Two rod-driven electroretinogram (ERG) components were recorded to monitor scotopic retinal signals during experimental manipulation of dopamine and gamma-aminobutyric acid (GABA) in normal cat eyes and in eyes pretreated with 6-hydroxydopamine (6-OHDA). The scotopic threshold response (STR) was elicited near absolute threshold to monitor signals traversing the rod pathway near quantal threshold; scotopic PII, which normally begins approximately 2 log units higher, was also monitored. Responses were evaluated by V-log I curves and criterion amplitudes after intravitreal drug injections into intact eyes in vivo. The depletion of dopaminergic cells by pretreating with 6-OHDA was confirmed histologically by immunocytochemical methods. 2. Dopamine abolished the STR and markedly decreased PII in the normal eye. Both 6-OHDA pretreatment and application of the dopamine antagonist, haloperidol, increased the STR amplitudes, but only for stimuli beginning 2 log units above threshold; PII amplitude also was increased. However, neither 6-OHDA pretreatment nor haloperidol affected the STR near absolute threshold. 3. Both GABA and bicuculline suppressed the STR in the normal eye. However, when applied to eyes pretreated with 6-OHDA or concurrent with haloperidol, bicuculline enhanced the STR. GABA enhanced the PII amplitude in the normal eye but had no effect in eyes pretreated with 6-OHDA or in the presence of haloperidol. 4. These results suggest that 1) dopaminergic activity modulates signals in the rod pathway at higher stimulus intensities but not near absolute threshold and 2) GABA can affect the scotopic PII component by acting through dopaminergic cells in the dark-adapted retina.