Does acetylcholine cause pupils to dilate? The real facts about how your pupils work

October 10, 2025 •

3 min read

Contrary to the common misconception, acetylcholine does not cause pupils to dilate. In fact, this vital neurotransmitter plays the central role in causing the pupils to constrict, a process known as miosis. This action is a key function of the body's parasympathetic nervous system, ensuring the eye can regulate the amount of light it receives.

Quick Summary

Acetylcholine is the primary neurotransmitter responsible for pupil constriction (miosis) through the parasympathetic nervous system. Pupil dilation (mydriasis) is caused by the opposing sympathetic nervous system, which utilizes norepinephrine.

Key Points

Acetylcholine causes pupil constriction (miosis), not dilation: The neurotransmitter activates the parasympathetic nervous system, leading to a smaller pupil.
Dilation (mydriasis) is controlled by the sympathetic nervous system: This opposing system releases norepinephrine to widen the pupil.
Different muscles in the iris are responsible for opposing actions: The circular iris sphincter muscle contracts to constrict the pupil, while the radial iris dilator muscle contracts to dilate it.
Anticholinergic drugs induce dilation: Medications like atropine block acetylcholine, preventing the sphincter muscle from contracting and thus leading to mydriasis.
Pupil size reflects the balance of the autonomic nervous system: The size of the pupil is a constant negotiation between the parasympathetic (constricting) and sympathetic (dilating) systems.
Cholinergic agonists are used to induce miosis: Drugs that mimic acetylcholine, like pilocarpine, are clinically used to constrict the pupil for treating conditions like glaucoma.

The Autonomic Nervous System and Pupil Control

The size of your pupils is meticulously controlled by the autonomic nervous system, which comprises two opposing branches: the parasympathetic and the sympathetic nervous systems. This delicate balance ensures that pupil size adjusts dynamically to changes in light, emotional state, and other stimuli.

Your eye's iris contains two sets of smooth muscles that control pupil size:

Iris Sphincter Muscle (or Constrictor Pupillae): This muscle is arranged in a circular pattern around the pupil. When it contracts, the pupil becomes smaller, a process called miosis.
Iris Dilator Muscle (or Dilator Pupillae): This muscle has fibers that extend radially, like spokes on a wheel. When it contracts, the pupil widens, a process called mydriasis.

The Role of Acetylcholine in Pupil Constriction (Miosis)

Acetylcholine's main function regarding pupil size is to cause constriction, not dilation. Here is how the process works:

Pathway Initiation: The pupillary constriction reflex is initiated by the parasympathetic branch of the autonomic nervous system. The signal originates in the brain, travels along the oculomotor nerve (cranial nerve III), and synapses in the ciliary ganglion, located behind the eyeball.
Acetylcholine Release: From the ciliary ganglion, postganglionic fibers release the neurotransmitter acetylcholine onto the iris sphincter muscle.
Receptor Activation: Acetylcholine binds to muscarinic receptors (specifically the M3 subtype) on the surface of the muscle cells.
Muscle Contraction: This binding triggers the sphincter muscle to contract, causing the pupil to become smaller and restricting the amount of light entering the eye. This is a crucial response in bright light to protect the retina from overexposure.

The Mechanism of Pupil Dilation (Mydriasis)

For the pupil to dilate, a different set of signals and a different neurotransmitter are required, controlled by the sympathetic nervous system.

Sympathetic Stimulation: When the body needs more light (e.g., in a dark environment or during a 'fight-or-flight' response), the sympathetic nervous system is activated.
Norepinephrine Release: Nerve fibers release norepinephrine, a neurotransmitter that acts on the iris dilator muscle.
Dilator Muscle Contraction: The radial fibers of the dilator muscle contract, pulling the iris outwards and causing the pupil to widen.

Pharmacological Manipulation of Pupillary Size

Medications can intentionally manipulate the balance of acetylcholine and norepinephrine to achieve either miosis or mydriasis for diagnostic and therapeutic purposes. Understanding these effects is critical in pharmacology.

Drugs That Influence Pupillary Response

Cholinergic Agonists: These drugs, such as pilocarpine eye drops, mimic the effects of acetylcholine. They cause the iris sphincter muscle to contract, leading to miosis. They are used in ophthalmology to treat conditions like certain types of glaucoma by increasing the outflow of aqueous humor.
Anticholinergic Drugs: These agents, including atropine and tropicamide, block muscarinic acetylcholine receptors. By preventing acetylcholine from acting on the sphincter muscle, they cause the pupil to dilate. This effect is commonly used during eye exams to allow a clear view of the retina.
Sympathomimetics: These drugs, like phenylephrine, mimic the sympathetic nervous system by stimulating alpha-adrenergic receptors on the dilator muscle. This causes mydriasis and can also be used for diagnostic purposes.

Comparison of Pupillary Control Pathways


Feature	Miosis (Constriction)	Mydriasis (Dilation)
Nervous System	Parasympathetic ('rest-and-digest')	Sympathetic ('fight-or-flight')
Key Neurotransmitter	Acetylcholine	Norepinephrine
Iris Muscle Involved	Sphincter Pupillae (circular)	Dilator Pupillae (radial)
Resulting Action	Muscle contracts, pupil narrows	Muscle contracts, pupil widens
Primary Stimulus	Bright light	Dim light, fear, excitement
Related Drug Class	Cholinergic Agonists (e.g., Pilocarpine)	Anticholinergic Drugs (e.g., Atropine)

Conclusion: Constriction, Not Dilation

In summary, it is a definitive fact that acetylcholine causes pupils to constrict, not dilate, as part of the parasympathetic nervous system's function. Pupil dilation is an opposite process driven by a different neurotransmitter, norepinephrine, under the control of the sympathetic nervous system. The intricate interplay between these two systems, mediated by their respective neurotransmitters, is what allows for the precise and constant regulation of pupil size. Pharmacologically, medications can target these pathways, either mimicking acetylcholine's effect to cause constriction or blocking it to induce dilation for medical purposes. For a deeper dive into the specific mechanisms, authoritative resources like the NCBI Bookshelf offer comprehensive physiological details on pupillary control.

Frequently Asked Questions

The primary action of acetylcholine on the pupils is to cause constriction, a process known as miosis. It achieves this by stimulating the iris sphincter muscle to contract.

Pupil constriction is managed by the parasympathetic nervous system. It sends signals to release acetylcholine, which then acts on the muscles controlling pupil size.

The neurotransmitter that causes pupil dilation (mydriasis) is norepinephrine, released by the sympathetic nervous system. It stimulates the iris dilator muscle to contract and widen the pupil.

Medications are used to block acetylcholine for various reasons. In ophthalmology, anticholinergic drops (like atropine) are used during eye exams to dilate the pupil so a doctor can better see the back of the eye.

Yes, medications known as cholinergic agonists, such as pilocarpine, mimic the effect of acetylcholine. They are used to cause pupil constriction, for example, in the treatment of glaucoma.

Mydriasis is the term for pupil dilation or widening, while miosis is the term for pupil constriction or narrowing. These opposing actions are controlled by the sympathetic and parasympathetic nervous systems, respectively.

Yes, different classes of drugs can cause opposite effects. For instance, opioids often cause pupil constriction (miosis), while stimulants like cocaine and amphetamines typically cause pupil dilation (mydriasis).