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The pupil is a hole in the centre of the iris, and its dilation is caused by two opposing muscles: the iris dilator and the iris sphincter. The iris dilator muscle, also known as the dilator pupillae muscle, is a smooth muscle of the eye that runs radially in the iris. It is innervated by the sympathetic nervous system, which acts by releasing noradrenaline, causing the muscle to contract and the pupil to dilate. The iris sphincter muscle, also known as the sphincter pupillae muscle, is located in the central parts of the iris and constricts the pupil. It is controlled by the parasympathetic nervous system and constricts the pupil when stimulated.
| Characteristics | Values |
|---|---|
| Name of the muscle | Iris dilator muscle, pupil dilator muscle, pupillary dilator, radial muscle of iris, radiating fibers, dilator pupillae muscle |
| Muscle type | Smooth muscle of the eye |
| Arrangement of cells | Spokelike arrangement of modified contractile cells called myoepithelial cells |
| Innervation | Postganglionic sympathetic nerves arising from the superior cervical ganglion as the sympathetic root of ciliary ganglion |
| Function | Contracts to pull the iris outward, widening the pupil and allowing more light to enter the eye |
| Controlled by | Sympathetic nervous system |
| Stimulated by | Arousal, fight-or-flight situation, adrenaline, anticholinergic agents, stimulant drugs, and some hallucinogenics |
| Related terms | Mydriasis, locus coeruleus neurotransmitter system, neuromodulator system, noradrenaline, anticholinergic agents, atropine, dilating drops |
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What You'll Learn
The iris dilator muscle
The dilator pupillae muscle is located in the outer parts of the iris, while the sphincter pupillae muscle is located in the central parts. The sphincter pupillae muscle constricts the pupil, causing it to become smaller. The constricting sphincter muscle receives input from brain systems involved in the pupillary light reflex.
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The iris sphincter muscle
The sphincter muscle fibres are slightly anterior to the pigmented epithelium of the iris. The iris sphincter muscle receives parasympathetic innervation via the short ciliary nerves, leading to pupillary constriction (miosis) and accommodation. The parasympathetic fibres that serve the sphincter muscle originate from the Edinger-Westphal nucleus of cranial nerve III. The signal synapses in the ciliary ganglia and become terminated on muscarinic receptors of the muscle fibres. The reciprocal function is primarily the responsibility of sympathetic innervation, which comes from the superior cervical ganglia. The sympathetic fibres help promote sphincter muscle relaxation, which is critical for periods of low light or night vision. Sympathetic innervation from the superior cervical ganglion projects to the dilator muscle of the iris via long ciliary nerves to control pupil dilation.
Adie syndrome, also known as Holmes-Adie syndrome, is a neuro-ophthalmological disorder characterised by a lack of response to light and a pupil that is tonically dilated but able to respond to accommodation. It results from damage to postganglionic fibres of the parasympathetic innervation to the eye, leading to an inability to constrict the iris sphincter muscle. Iridoplegia is the paralysis of the sphincter muscle of the iris, often resulting from direct trauma to the orbit but also from inflammation or eyedrops.
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Locus coeruleus noradrenaline neurons
Pupil dilation is caused by two antagonistic muscles: the dilator pupillae and the sphincter pupillae. The former is located in the outer parts of the iris and dilates the pupil, while the latter is located in the central parts and constricts it. The dilator muscle is innervated by the sympathetic nervous system, which acts by releasing noradrenaline, causing the muscle to contract and the pupil to dilate.
The locus coeruleus (LC) is a nucleus in the pons of the brainstem that is the principal site for brain synthesis of norepinephrine (noradrenaline). It is composed of mostly medium-sized neurons, with 22,000 to 51,000 total pigmented neurons in adult humans. The LC-noradrenaline system modulates cortical, subcortical, cerebellar, brainstem, and spinal cord circuits. Norepinephrine released from the LC will feedback to inhibit its production, while corticotropin-releasing factor will feedback to inhibit its production and positively feed into the LC to increase norepinephrine production.
The LC is involved in physiological responses to stress and panic and is related to clinical depression, panic disorder, Parkinson's disease, Alzheimer's disease, and anxiety. Locus coeruleus noradrenaline neurons are proposed to be the core region that induces pupil dilation. This is supported by a monkey electrophysiological study that reported that neural activation in the LC precedes pupil dilation, and that electrical stimulation at this site induces pupil dilation. In addition, brain imaging studies on humans have reported that neural activity in the LC is positively correlated with pupil diameter.
The LC's role in cognitive function in relation to stress is complex and multi-modal. Norepinephrine released from the LC can act on α2 receptors to increase working memory, but an excess of NE may decrease working memory by binding to lower-affinity α1 receptors. Psychiatric research has documented that enhanced noradrenergic postsynaptic responsiveness in the neuronal pathway that originates in the LC and ends in the basolateral nuclear complex of the amygdala is a major factor in the pathophysiology of most stress-induced fear-circuitry disorders, especially post-traumatic stress disorder (PTSD).
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Pupillary response
The pupil constrictor muscle (or sphincter pupillae muscle) is located in the central parts of the iris and constricts the pupil. The constricting sphincter muscle receives input from brain systems involved in the pupillary light reflex. The iris sphincter muscle, which is under the control of the parasympathetic pathway, is quickly modulated by the neuromodulator system.
The dilator muscle is innervated by the sympathetic nervous system. It receives signals from the neuromodulator system with slow latency and is involved in maintaining sustained pupil dilation. Sympathetic output, associated with arousal, stimulates the iris dilator muscle to constrict, opening our pupils during a fight-or-flight situation.
The constriction response (miosis) is the narrowing of the pupil, which may be caused by scleral buckles or drugs such as opiates, opioids, or anti-hypertension medications. Constriction of the pupil occurs when the circular muscle, controlled by the parasympathetic nervous system (PSNS), contracts, and also to an extent when the radial muscle relaxes.
A dilation response (mydriasis) is the widening of the pupil and may be caused by adrenaline, anticholinergic agents, stimulant drugs such as MDMA, cocaine, and amphetamines, and some hallucinogenics such as LSD. Dilation of the pupil occurs when the smooth cells of the radial muscle, controlled by the sympathetic nervous system (SNS), contract, and also when the cells of the iris sphincter muscle relax.
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Sympathetic and parasympathetic output
The pupil is controlled by two antagonistic muscles: the dilator pupillae, which dilates the pupil, and the sphincter pupillae, which constricts it. The dilator pupillae is innervated by the sympathetic nervous system, while the sphincter pupillae is innervated by the parasympathetic nervous system.
The sympathetic nervous system is activated by light, pain, and wakefulness. When stimulated, it contracts the dilator pupillae, widening the pupil and allowing more light to enter the eye. This response is particularly associated with the fight-or-flight response, where more light can reach the retina. The sympathetic branch, mediated by posterior hypothalamic nuclei, directly stimulates the dilator muscles to produce pupil enlargement. The sympathetic output is controlled by separate light-inhibited and light-stimulated pathways. The light-inhibited pathway originates in the retina-receptive neurons of the pretectum and suprachiasmatic nucleus (SCN). The light-stimulated pathway is less obvious since it is masked by sympatho-inhibition evoked by light.
The parasympathetic nervous system is also activated by light, which stimulates the light reflex. This system is responsible for pupil constriction via activation of the sphincter pupillae muscle. The contribution of the parasympathetic pathway is mediated by central inhibition of the Edinger-Westphal complex of the oculomotor nucleus in the midbrain. The parasympathetic output is controlled by a light-stimulated pathway.
The relative contributions of the sympathetic and parasympathetic systems on pupillary responses may differ depending on the context. Higher luminance levels lead to greater activation of the parasympathetic system, resulting in pupil constriction, while lower luminance levels lead to greater activation of the sympathetic system, resulting in pupil dilation. However, pupil dilation evoked by emotional auditory stimuli was observed to be greater in a dark environment compared to a bright one. This suggests that arousal-induced pupil dilation is primarily mediated by sympathetic activation.
Pupil dilation is also observed during cognitive processing, with larger dilation occurring under demanding task conditions. The specific contribution of sympathetic or parasympathetic activity to cognitive activities is unclear. However, studies suggest that pupil dilation related to task difficulty is mainly mediated by inhibition of the parasympathetic pathway.
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Frequently asked questions
The dilator pupillae muscle, also known as the iris dilator muscle, dilates the pupil.
The dilator pupillae muscle is a ring of contractile cells within the iris that facilitates pupillary dilation (mydriasis).
The dilator pupillae muscle contracts, widening the pupil and allowing more light to enter the eye.
The dilator pupillae muscle is innervated by the sympathetic nervous system. When stimulated, the muscle contracts, causing the pupil to dilate.
The opposite of the dilator pupillae muscle is the sphincter pupillae muscle, which constricts the pupil.
