Located between vessels of the choriocapillaris and light-sensitive outer segments of the photoreceptors, the retinal pigment epithelium (RPE) closely interacts with photoreceptors in the maintenance of visual function. Increasing knowledge of the multiple functions performed by the RPE improved the understanding of many diseases leading to blindness. This review summarizes the current knowledge of RPE functions and describes how failure of these functions causes loss of visual function. Mutations in genes that are expressed in the RPE can lead to photoreceptor degeneration. On the other hand, mutations in genes expressed in photoreceptors can lead to degenerations of the RPE. Thus both tissues can be regarded as a functional unit where both interacting partners depend on each other.

The Retinal Pigment Epithelium in Visual Function

Mammalian circadian rhythms are controlled by endogenous biological oscillators, including a master clock located in the hypothalamic suprachiasmatic nuclei (SCN). Since the period of this oscillation is of approximately 24 h, to keep synchrony with the environment, circadian rhythms need to be entrained daily by means of Zeitgeber ("time giver") signals, such as the light-dark cycle. Recent advances in the neurophysiology and molecular biology of circadian rhythmicity allow a better understanding of synchronization. In this review we cover several aspects of the mechanisms for photic entrainment of mammalian circadian rhythms, including retinal sensitivity to light by means of novel photopigments as well as circadian variations in the retina that contribute to the regulation of retinal physiology. Downstream from the retina, we examine retinohypothalamic communication through neurotransmitter (glutamate, aspartate, pituitary adenylate cyclase-activating polypeptide) interaction with SCN receptors and the resulting signal transduction pathways in suprachiasmatic neurons, as well as putative neuron-glia interactions. Finally, we describe and analyze clock gene expression and its importance in entrainment mechanisms, as well as circadian disorders or retinal diseases related to entrainment deficits, including experimental and clinical treatments.

/pdf/physiology-of-circadian-entrainment-2sprglw0dp.pdf

Physiology of circadian entrainment.

Melatonin receptors: Localization, molecular pharmacology and physiological significance

Vanecek, Jiri. Cellular Mechanisms of Melatonin Action. Physiol. Rev. 78: 687–721, 1998. — The pineal hormone melatonin is involved in photic regulations of various kinds, including adaptation to l...

Cellular Mechanisms of Melatonin Action

1 Compound Eyes and the World of Vision Research.- 2 Autrum's Impact on Compound Eye Research in Insects.- 3 Optics and Evolution of the Compound Eye.- 4 Photoreceptor Optics, Theory and Practice.- 5 Variations in the Structure and Design of Compound Eyes.- 6 Visual Pigments of Compound Eyes - Structure, Photochemistry, and Regeneration.- 7 Distribution of Insect Visual Chromophores: Functional and Phylogenetic Aspects.- 8 Pigments in Compound Eyes.- 9 Phototransduction in Limulus Ventral Photoreceptors: Roles of Calcium and Inositol Trisphosphate.- 10 The Retina-Lamina Pathway in Insects, Particularly Diptera, Viewed from an Evolutionary Perspective.- 11 Coding Efficiency and Design in Visual Processing.- 12 Neurotransmitters in Compound Eyes.- 13 Circadian Rhythms in the Invertebrate Retina.- 14 Color Vision in Honey Bees: Phenomena and Physiological Mechanisms.- 15 Polarization Sensitivity in Compound Eyes.- 16 Beneath the Compound Eye: Neuroanatomical Analysis and Physiological Correlates in the Study of Insect Vision.- 17 Directionally Selective Motion Detection by Insect Neurons.- 18 Neural Mechanisms of Visual Course Control in Insects.- 19 Size and Distance Perception in Compound Eyes.

Facets of Vision

In lower vertebrates, cone retinomotor movements occur in response to changes in lighting conditions and to an endogenous circadian clock. In the light, cone myoids contract, while in the dark, they elongate. In order to test the hypothesis that melatonin and dopamine may be involved in the regulation of cone movement, we have used an in vitro eyecup preparation from Xenopus laevis that sustains light- and dark-adaptive cone retinomotor movement. Melatonin mimics darkness by causing cone elongation. Dark- and melatonin-induced cone elongation are blocked by dopamine. Dopamine also stimulates cone contraction in dark-adapted eyecups. The effect of dopamine appears to be mediated specifically by a dopamine receptor, possibly of the D2 type. The dopamine agonist apomorphine and the putative D2 agonist LY171555 induced cone contraction. In contrast, the putative D1 agonist SKF38393-A and specific alpha 1-, alpha 2-, and beta-adrenergic receptor agonists were without effect. Furthermore, the dopamine antagonist spiroperidol not only blocked light-induced cone contraction, but also stimulated cone elongation in the light. These results suggest that dopamine is part of the light signal for cone contraction, and that its suppression is part of the dark signal for cone elongation. Melatonin may affect cone movement indirectly through its influence on the dopaminergic system.

/pdf/circadian-regulation-of-retinomotor-movements-i-interaction-28v9d7a8z4.pdf

Circadian regulation of retinomotor movements. I. Interaction of melatonin and dopamine in the control of cone length.

Chapter 2 Regulation of rhythmic photoreceptor metabolism: A role for post-receptoral neurons

Melatonin and rhythmic photoreceptor metabolism: melatonin-induced cone elongation is blocked at high light intensity.

Melatonin and dopamine interactions in the regulation of rhythmic photoreceptor metabolism1

Cone photoreceptor movements in lower vertebrates are regulated by the interaction of the light-dark cycle and an endogenous circadian clock. We have suggested that melatonin and dopamine interact to regulate dark- and light-adaptive movements, respectively, and that melatonin affects cones indirectly by inhibiting dopamine release. In fact, any factor modulating dopaminergic neurons in the retina may have effects on either cone elongation or contraction. We have utilized an in vitro eyecup preparation from the African clawed frog, Xenopus laevis, to evaluate a possible role of the neurotransmitter GABA, which is thought to tonically suppress dopamine release. GABA agonists mimic the effects of darkness and induce cone elongation; the effects of GABA agonists are blocked by dopamine. Muscimol-induced cone elongation occurs at low light intensity but is inhibited by bright light in eyecups prepared from cyclic-light-maintained animals. Although neither melatonin nor muscimol stimulates cone elongation in bright light, simultaneous application of both drugs induces elongation. The GABA antagonist picrotoxin induces cone contraction which is blocked by the dopamine receptor antagonist spiroperidol, which suggests that GABA may affect cone movement in Xenopus by regulating dopamine neurons. Consistent with this, picrotoxin-induced cone contraction is Ca+2 dependent and is blocked by high Mg+2 or the Ca+2 antagonist nifedipine. Pharmacological analysis suggests that the effects of GABA may result from its action at more than one receptor subtype. Our results support the hypothesis that dopamine is part of the light signal for cone contraction and that its suppression is part of the signal for cone elongation.

Circadian regulation of retinomotor movements: II. The role of gaba in the regulation of cone position

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