SRIF effects mediated by sst
1 were confined to
innermost retinal portions, and, as discussed, involved two different
populations of amacrine cells (one of which is represented by TH-IR
amacrines), the SRIF displaced amacrines, and some GCs. Regarding
possible actions of SRIF onto dopaminergic cells, potent stimulatory
effects of SRIF on DA release in the rat striatum have been
reported
54 ; however, this effect seems to be mediated by
sst
2.
55 SRIF control of dopaminergic
amacrines is likely both in rat and in rabbit retinas, but rat and
rabbit clearly differ in the specific sst that mediates control.
Whereas in rat retinas dopaminergic amacrines express
sst
2A but not
sst
1,
23 in rabbit retinas TH-IR
amacrines seem not to express
21 or to express only
partially
22 sst
2A, whereas they
express sst
1. It is interesting to note that the
effects of SRIF on rabbit GCs are similar to dark
adaptation,
17 whereas DA, with an extracellular level that
increases with increasing ambient light intensity, is involved in light
adaptation.
56 As previously suggested,
17 SRIF
may be released in the dark and, therefore, it may act through
sst
1 on rabbit dopaminergic amacrines as a dark
signal, resulting in inhibition of DA release. This is consistent with
observations of the chicken retina where amacrine cells coexpressing
enkephalin, neurotensin, and SRIF are active in the dark and inhibit
dopaminergic amacrines.
19 In contrast, in rat retinas,
SRIF action on dopaminergic amacrines through
sst
2A could stimulate DA release, as in the rat
striatum.
55 This hypothesis suggests different mechanisms
for dark–light adaptation in rat and in rabbit retinas that may be
related to the remarkable differences in diurnal activity patterns of
rats and rabbits. Functional data on the effects of SRIF in the rat
retina would shed some light on this issue.