Abstract
The retina is a complex, but well-organized neural structure that converts optical radiation into neural signals that convey photic information to a wide variety of brain structures. The present paper is concerned with the neural circuits underlying phototransduction for the central pacemaker of the human circadian system. The proposed neural framework adheres to orthodox retinal neuroanatomy and neurophysiology. Several postulated mechanisms are also offered to account for the high threshold and for the subadditive response to polychromatic light exhibited by the human circadian phototransduction circuit. A companion paper, modeling circadian phototransduction: Quantitative predictions of psychophysical data, provides a computational model for predicting psychophysical data associated with nocturnal melatonin suppression while staying within the constraints of the neurophysiology and neuroanatomy offered here.
Highlights
In humans, like all other mammals and many other species, the orchestration of physiology and behavior to the natural light-dark cycle is governed by a tight neural coupling of the phototransduction mechanisms in the retina with the master clock in the brain
All authors contributed to the article and approved the submitted version
Summary
Like all other mammals and many other species, the orchestration of physiology and behavior to the natural light-dark cycle is governed by a tight neural coupling of the phototransduction mechanisms in the retina with the master clock in the brain. For wavelengths shorter than 500 nm, it is postulated that the ipRGCs signal would reflect both its intrinsic photosensitive response and the SB input through the en passant synapses (Dumitrescu et al, 2009) For these short wavelengths, rod shunting inhibition would be reduced by the SB input to the AII amacrine plexus (Process A in Figure 1; Demb and Singer, 2012). It can only signal the “yellow” OFF response from the spectrally opponent SB, which decouples the shunting inhibition of the M1 ipRGCs by the AII amacrine These postulated amacrine mechanisms (Processes A–C in Figure 1) controlling rod shunting inhibition were part of the FIGURE 2 | Model predictions of the spectral sensitivity of the circadian phototransduction circuit when exposed to either monochromatic (narrow-band) or polychromatic light sources at 300 scotopic lx at the eye. But consistent suggestion with that offered here for the SCA, the A18 amacrine may play a similar role of maintaining the strictly ON pathway for the M1d ipRGCs
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