How it Works
This simulation models phototransduction using the Naka-Rushton equation combined with calcium-mediated adaptation. In darkness, high cGMP keeps CNG channels open (dark current). Light activates PDE via the G-protein cascade, hydrolyzing cGMP, closing channels, and hyperpolarizing the cell.
Adaptation is implemented via a sliding sensitivity variable that tracks background light intensity according to Weber's law. The threshold scales proportionally to background, demonstrating why we can see detail both at dusk and in bright sunlight.
σ_adapted = σ₀ · (1 + I_bg/I_D) [Weber adaptation]
dcGMP/dt = α_syn/(1 + Ca²⁺/K_Ca) − β·PDE·cGMP
V_m = V_dark + ΔV·(1 − cGMP/cGMP_dark)
Frequently Asked Questions
What is phototransduction?
Phototransduction is the process by which photoreceptor cells (rods and cones) convert light into electrical signals. A photon activates rhodopsin, which activates transducin (a G-protein), leading to phosphodiesterase activation, cGMP hydrolysis, channel closure, and hyperpolarization of the cell.
What is the difference between rods and cones?
Rods are highly sensitive and operate in dim light (scotopic vision); they contain rhodopsin and respond to a broad wavelength range but do not distinguish color. Cones operate in bright light (photopic vision), contain opsins tuned to different wavelengths (S, M, L), and enable color discrimination and high acuity.
What is the Weber-Fechner law?
The Weber-Fechner law states that the just-noticeable difference (JND) in stimulus intensity is proportional to the background intensity: ΔI/I = k (Weber's law). Fechner extended this to a logarithmic relationship: perceived sensation S = k·log(I/I₀). This explains why adaptation raises the detection threshold in proportion to background light.
How do photoreceptors adapt to different light levels?
Photoreceptors use several mechanisms: bleaching (rhodopsin is consumed in bright light, reducing sensitivity), calcium feedback (Ca²⁺ regulates guanylate cyclase, restoring cGMP), and slow pigment regeneration. This allows vision across ~10 log units of light intensity.
What is the role of cGMP in photoreception?
In darkness, cGMP keeps cyclic nucleotide-gated (CNG) channels open, allowing Na⁺ and Ca²⁺ to flow in (the 'dark current'). Light activates phosphodiesterase, which hydrolyzes cGMP, causing CNG channels to close, stopping the dark current, and hyperpolarizing the cell, which reduces glutamate release.
What is the Naka-Rushton equation?
The Naka-Rushton equation describes photoreceptor response: R/Rmax = I^n / (I^n + σ^n), where R is the response, I is light intensity, σ is the semi-saturation constant (intensity at half-max response), and n is the Hill coefficient controlling the slope of the curve.
How does dark adaptation work?
Dark adaptation occurs after exposure to bright light. First, cones recover sensitivity over ~10 minutes. Then rods regenerate rhodopsin (from retinal + opsin) over ~30-40 minutes, producing the characteristic two-phase dark adaptation curve with a 'rod-cone break' around 10 minutes.
Why is the fovea rod-free?
The fovea centralis, the area of highest visual acuity, contains only cones (no rods). This allows for high-resolution color vision in daylight. The absence of rods means the fovea is actually less sensitive to very dim light than the peripheral retina, which has more rods.
What is the spectral sensitivity of the three cone types?
Human cones come in three types: S-cones (peak ~420 nm, blue), M-cones (peak ~530 nm, green), and L-cones (peak ~560 nm, red). Color perception arises from comparing the responses across these three channels (trichromacy).
What causes night blindness?
Night blindness (nyctalopia) is caused by deficiencies in rod photoreceptor function. Common causes include vitamin A deficiency (retinal is derived from vitamin A), mutations in rhodopsin or other phototransduction proteins, and retinitis pigmentosa (progressive rod degeneration).