The autonomic nervous system controls involuntary functions (heart rate, digestion, pupil size) through sympathetic (fight-or-flight) and parasympathetic (rest-and-digest) divisions with opposing effects on most organs. Sympathetic neurons release norepinephrine; parasympathetic neurons release acetylcholine. The balance between these divisions maintains homeostatic stability.
From your study of synaptic transmission, you understand how neurons communicate through neurotransmitter release at synapses. The autonomic nervous system (ANS) applies this machinery to control the body's internal organs — heart, lungs, gut, blood vessels, glands — without conscious effort. It is the neural infrastructure of homeostasis, continuously adjusting organ function to match the body's changing demands.
The ANS is organized into two divisions with largely opposing effects. The sympathetic division prepares the body for action — the classic "fight-or-flight" response. When activated, it increases heart rate and contractile force, dilates bronchioles to increase airflow, redirects blood from the gut to skeletal muscles, dilates pupils, and triggers glucose release from the liver. The parasympathetic division does roughly the opposite — the "rest-and-digest" response. It slows the heart, constricts bronchioles, stimulates digestive secretions and gut motility, and constricts pupils. Most organs receive input from both divisions, and the body's moment-to-moment physiological state reflects the balance between them, not the action of one alone. Your resting heart rate, for example, is not an intrinsic property of the heart — it is set by tonic parasympathetic slowing via the vagus nerve. Block the vagus, and heart rate jumps from ~70 to ~100 beats per minute.
Both divisions share a common two-neuron architecture: a preganglionic neuron in the central nervous system synapses onto a postganglionic neuron in a peripheral ganglion, which then innervates the target organ. The key pharmacological difference lies in the neurotransmitters used. All preganglionic neurons — both sympathetic and parasympathetic — release acetylcholine (ACh) at nicotinic receptors in the ganglion. But the postganglionic neurons differ: parasympathetic postganglionic neurons release ACh at muscarinic receptors on target organs, while sympathetic postganglionic neurons release norepinephrine (NE) at adrenergic receptors. This distinction explains why drugs targeting these receptor systems have such specific physiological effects — atropine (a muscarinic antagonist) blocks parasympathetic output, causing elevated heart rate and dry mouth, while beta-blockers reduce sympathetic drive to the heart.
The two divisions also differ anatomically. Sympathetic preganglionic neurons originate from the thoracic and lumbar spinal cord and synapse in paravertebral ganglia close to the spine, sending long postganglionic fibers to distant targets — an arrangement that enables rapid, coordinated whole-body activation. Parasympathetic preganglionic neurons originate from brainstem nuclei (via cranial nerves III, VII, IX, and X) and sacral spinal cord, with long preganglionic fibers that synapse in ganglia near or within the target organs, allowing more localized, organ-specific control. This is why sympathetic activation tends to be diffuse — a global alarm signal — while parasympathetic effects are more targeted and graded.