![]() In mice, transient changes in luminance may be detected directly by melanopsin-expressing cells in the iris sphincter muscle to drive pupil constriction, instead of through the rod photoreceptor pathway ( Wang et al., 2017). ![]() Rods adapt under sustained illumination, under which conditions pupil diameter is controlled by the melanopsin-expressing retinal ganglion cells, which are intrinsically photosensitive and display little adaptation ( Keenan et al., 2016). Cells of the pretectal olivary nucleus drive pupil constriction via projections onto cholinergic preganglionic motoneurons in the E–W nucleus ( Beatty and Lucero-Wagoner, 2000 May et al., 2008). In primates, transient changes in luminance are reflected in the activity of rod photoreceptors and are relayed to melanopsin-expressing retinal ganglion cells that project to the pretectal olivary nucleus ( Clarke and Ikeda, 1985 Gamlin et al., 1995). Two retinal mechanisms are thought to be involved in detecting the changes in luminance that control pupil diameter. The pupillary light response is thought to optimize retinal illumination and, thereby, visual perception. 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. Lesions in parasympathetic pathways primarily affect the pupillary light response. Sympathetic nervous activity promotes dilation and parasympathetic activity promotes constriction of the pupil, but changes in pupil diameter driven by changes in luminance and arousal engage sympathetic and parasympathetic nervous systems differentially, with lesions in sympathetic pathways primarily impeding dilation in response to changes in arousal, but not luminance ( Loewenfeld, 1958). The iris sphincter and dilatory pupil muscles are under the control of the parasympathetic and sympathetic nervous systems, respectively. Activity of projecting neurons in the E-W nucleus drives contraction of the iris sphincter muscle and constriction of the pupil inhibition of E-W neurons relaxes the iris sphincter muscle, permitting dilation (Figure 1A). The iris sphincter muscle is controlled via cholinergic preganglionic motoneurons in the Edinger–Westphal (E–W) nucleus, which project to the ciliary ganglion of the third cranial nerve from which the iris sphincter muscle is controlled via the ciliary nerve ( Beatty and Lucero-Wagoner, 2000). The iris sphincter muscle is stronger than the dilatory pupillary muscle, making the iris sphincter muscle the primary controller of pupil diameter. The diameter of the pupil is controlled by the iris sphincter muscle that constricts the pupil and the dilatory pupillary muscle that promotes pupil dilation ( Borgdorff, 1975 Levin and Kaufman, 2011). Pupil dilation is altered by luminance in the visual environment as well as during arousal, defined here as periods of heightened sensory responsiveness and perception that involve autonomic and endocrine activation. Mechanisms Controlling Pupil Diameter and the Effects of Luminance Here we review evidence that changes in pupil dilation reflect and, in some instances, may be caused by the activity of neuromodulatory pathways. It has been suggested that these changes are linked by the activities of neuromodulatory systems ( Jones, 2004 Lee and Dan, 2012) and changes in the activity of noradrenergic and cholinergic circuitry correlate with changes in pupil dilation. As a result of these correlations, pupillometry has been used as an indirect measure of brain state.Ĭhanges in the behavior of an animal, the pupil dilation (mydriasis), and the brain state often coincide on the scale of seconds. Changes in network activity are often accompanied by changes in neuronal responsiveness and pupil diameter ( McGinley et al., 2015). Similarly, sharp wave ripples are observed in hippocampus during periods of reduced activity such slow wave sleep, quiet wakefulness, and grooming ( Buzsáki, 1986). For example, high frequency fluctuations in pyramidal cell membrane potential, local field potential (LFP), and electroencephalogram (EEG) are observed in sensory cortices during attentive or activated states ( Steriade, 1997 Crochet and Petersen, 2006). Brain states can be defined as periods of neuronal network activity that correlate with behaviors such as periods of arousal, locomotion, exploration, and attention ( Lee and Dan, 2012). An animal's behavior and neuronal responses are modulated by changes in brain state.
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