Pupil constriction parasympathetic1/27/2024 ![]() ACh, acetylcholine ON, overnight PSR, pupil stimulus response. (D, H) Normalized pupil sizes in response to 480 nm light exposure (D) and ACh activation (H) after incubation ON in Tyrode's solution alone, or in addition to carbenoxolone (added 1 hour before stimulation) over 10 minutes. (B, C, F, G) Normalized pupil sizes in response to 480 nm light exposure (B, C) and ACh activation (G, F) after incubation ON in Tyrode's solution alone, or together with verapamil (added 1 hour before stimulation), Ca 2+-free medium (incubated ON), and Ca 2+-free medium (exchanged 1 hour before stimulation) over 1 min (B, F) and 10 minutes (C, G). (A–E) Normalized pupil sizes of enucleated eyes in response to 480 nm light stimulation (A) and ACh activation (E) after incubation ON in Tyrode's solution alone, or together with 2-APB (added 1 hour before stimulation), 4-CP (added 1 hour before stimulation), over 10 minutes. Together, this study presents new mechanisms regulating synchronized pupil dilation and contraction, sustained pupil constriction, iridal stimulation-contraction coupling, and pupil escape.ĭetermination of the Ca 2+ dynamics that mediate the pupil stimulus response. ![]() The parasympathetic portion of this bilateral nucleus (Edinger-Westphal nucleus in humans) is located rostral and medial to the motor nucleus of cranial nerve III at the level of the rostral. The oculomotor nuclei are located in the rostral mesencephalon (midbrain). Furthermore, pupil escape is driven by membrane potential hyperpolarization where voltage-gated potassium channels play a crucial role. This parasympathetic portion of this nerve controls pupillary constriction. Stimulation of the parasympathetic nervous system results in: Constriction of pupils Decreased heart rate and blood pressure Constriction of bronchial muscles Increase in digestion Increased production of saliva and mucus Increase in urine. The pupillary light response is thought to optimize retinal illumination and, thereby, visual perception. Moreover, the degree of membrane potential repolarization in the dark is correlated with the latency and velocity of iridal constriction. The parasympathetic nervous system decreases respiration and heart rate and increases digestion. The diameter of the pupil is modulated by changes in luminance, with dilation of the pupil in low light conditions and constriction in bright light, the latter referred to as the pupillary light response. Both local and parasympathetic iridal activations are necessary, but not sufficient for sustained pupil constriction. The use of pupillometry recordings captured the relaxation, contraction, and pupil escape (redilation) processes for 10 minutes up to 1 hour.Īmong others, our results show that ryanodine receptor channels are the main driver for iridal stimulation-contraction coupling, in which extracellular influx of Ca2+ is required for amplification of pupil constriction. In this study, the PLR was examined in mouse enucleated eyes ex vivo in real-time under different ionic conditions in response to acetylcholine and/or blue light (480 nm). To better understand the cellular mechanisms that regulate pupil physiological dynamics via central and local photoreception, we have examined the regulation of the PLR via parasympathetic and local activation, respectively. In mammals, pupil constriction and dilation form the pupillary light reflex (PLR), which is mediated by both brain-regulated (parasympathetic) and local iris-driven reflexes.
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