The retinae of lower vertebrates undergo a number of structural changes during light adaptation, including the photomechanical contraction of cone myoids and the dispersion of melanin granules within the epithelial pigment. Since the application of dopamine to dark-adapted retinae is known to produce morphological changes that are characteristic of light adaptation, dopamine is accepted as a casual mechanism for such retinomotor movements. However, we report here that in the teleost fish, Aequidens pulcher, the intraocular injection of 6-hydroxydopamine (6-OHDA), a substance known to destroy dopaminergic retinal cells, has no effect on the triggering of light-adaptive retinomotor movements of the cones and epithelial pigment and only slightly depresses the final level of light adaptation reached. Furthermore, the retina continues to show circadian retinomotor changes even after 48 h in continual darkness that are similar in both control and 6-OHDA injected fish. Biochemical assay and microscopic examination showed that 6-OHDA had destroyed dopaminergic retinal cells. We conclude, therefore, that although a dopaminergic mechanism is probably involved in the control of light-induced retinomotor movements, it cannot be the only control mechanism, nor can it be the cause of circadian retinomotor migrations. Interestingly, 6-OHDA injected eyes never reached full retinomotor dark adaptation, suggesting that dopamine has a role to play in the retina's response to darkness.

We have investigated the effects of light and dark adaptation on the overall morphology of bipolar cell (BC) terminals in sublaminae a and b of the inner plexiform layer after labelling with Lucifer Yellow (LY) and PKC immunostaining using confocal laser scanning microscopy and serially sectioned material for electron microscopy. Three-dimensional reconstructed terminals showed marked adaptation-dependent changes of their morphology. Terminals of mixed rod-cone BCs in sublamina a (Ma BC) were irregular and scalloped in light adapted, but smooth and regular in dark-adapted specimens. Terminals from mixed rod-cone BCs in sublamina b (Mb BCs) exhibited an opposite behaviour. At the ultrastructural level, bipolar terminals in both sublaminae showed fingerlike extensions (spinules) invaginating presynaptic amacrine cell (AC) processes. Sixty-two percent of the dark-adapted Mb terminals in sublamina b showed spinules, whereas 21% of the light-adapted terminals had spinules. By contrast, 50.6% of the light-adapted Ma terminals in sublamina a formed spinules, compared to 17.8% of the dark-adapted Ma terminals in this sublamina. These observations reflect the functional subdivision of the inner plexiform layer in an inner ON-and an outer OFF-centre lamina. Our findings suggest that the synaptic plasticity of BC axon terminals may be due to differences of BC membrane potential, or the activity of AC input onto bipolar terminals. They may contribute to processes of fine tuning regulating the efficiency of AC-BC interaction under varying adaptation conditions.

We chose synaptic terminals of rat rod bipolar cells as a model system to study activity-related changes in the overall morphology and the fine structure of synaptic sites. Using confocal laser scanning microscopy in conjunction with three-dimensional reconstruction and electron microscopy, we examined the effect of light and dark adaptation on axon terminals identified by protein kinase C (PKC) immunoreactivity. Rod bipolar cell axon terminals consisted of 2-3 polymorphic boutons situated close to the ganglion cell layer and a single ovoid swelling located more distally. Both components of the terminal complex showed adaptation-dependent differences in the distribution of PKC immunoreactivity and in their morphology. In light-adapted rod bipolar cell axon terminals, PKC immunoreactivity was homogeneously distributed throughout the cytoplasm, whereas terminals from dark-adapted animals showed PKC immunoreactivity preferentially localised in the submembrane compartment and a reduced staining of the more central cytoplasm. In three-dimensional reconstructions of optical sections and at the ultrastructural level, the shape of light-adapted axon terminals was round and smooth and exhibited more convexly curved synaptic membranes. In contrast, dark-adapted terminals had irregular contours, numerous dimples and a concave synaptic curvature. No spinules of bipolar cell terminals were observed in dark-adapted material. These observations are discussed in the context of activity-related morphological plasticity of central nervous system synapses and of the functions of PKC in the cycle of vesicle fusion and retrieval at the tonically active ribbon synapses of the rod bipolar axon terminal.

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