The retinal dark-light switch may provide signals which trigger global changes within the retina (Morgan & Boelen, 1996). Dopamine is well-described as a light adaptive signal in the retina (Witkovsky & Dearry, 1992), and dopamine is the predominant transmitter released in the light in the retinal dark-light switch. I examined the localisation of the D1-like dopamine receptors using immunohistochemical techniques in chicken retina. A clear band of D1-receptor-like labelling was seen on the outer plexiform layer, as well as cellular staining in the inner nuclear layer, probably a subset of horizontal, amacrine, possibly interplexiform and occasional displaced ganglion cells. The inner plexiform layer was extensively labelled, as was a subset of somata in the ganglion cell layer. These localisations of D1-receptors were generally consistent with the known D1-dopaminergic function in the retina. However, D1-receptors were not detected on the somata of ENSLI amacrine cells, in contrast to the predicted localisation from the functional data incorporated into the retinal dark-light switch.

Based on observations from other tissues, the receptors for transmitters released from the retinal dark-light switch may have a common signal transduction pathway, affecting cAMP levels. I only detected slight, but significant increases in cAMP levels at light onset. No other light- or dark- induced changes in cAMP levels were detected.

The responses of cAMP levels to the transmitters of the retinal dark-light switch were examined in isolated chicken retina. Melatonin and a D2-receptor agonist, quinpirole suppressed cAMP levels, while enkephalin, neurotensin, somatostatin and a D1-agonist, SKF38393 increased cAMP levels. The peptide-induced changes in cAMP levels did not reflect the expected inhibitory coupling to adenylate cyclase.

A membrane preparation enabled direct receptor-induced changes in the levels of cAMP to be measured. The responses to melatonin and the dopamine agonists were similar in direction to those seen in whole retina. However, enkephalin caused both increases and decreases in cAMP levels, presumably due to interactions with at least two receptor types with opposing coupling to adenylate cyclase. Neurotensin suppressed forskolin-stimulated levels of cAMP. The absence of a change in cAMP levels with somatostatin suggested that retinal somatostatin receptors may not be coupled to adenylate cyclase.

The slow inactivating L-type calcium channels have been associated with synaptic transmission in the retina, modulate the synthesis and release of melatonin in photoreceptors and are a potential site for modulation by dopamine-regulated phosphorylation. I investigated the immunocytochemical localisation of the known neuronal a1-subunits of L-type calcium channels to provide insights into their signalling roles in the retina. The a1-subunits of these calcium channels were differentially localised. An a1-c-like subunit was predominantly localised on Müller cells. Most neuronal somata were labelled with an a1-d-like subunit antibody. The predominant a1-f-like subunit staining was on photoreceptor terminals, and there was fainter labelling of somata in amacrine and ganglion cell layers and two bands in the inner plexiform layer.