Anatomical features and fiber pathways
The parasympathetic division has a distinct focal localization. The cell bodies of preganglionic neurons lie in two unconnected zones:
- Brainstem: nuclei lie among the motor neurons of the cranial nerves. Fibers of the III (oculomotor), VII (facial), and IX (glossopharyngeal) nerves travel to the head ganglia, innervating the sphincter pupillae, ciliary muscle, and salivary glands. Fibers of the X nerve (n. vagus) descend to the organs of the thoracic and upper abdominal cavities.
- Spinal cord: nuclei are located in the gray matter of the sacral segment. Their axons form the pelvic nerves, which innervate the lower abdominal cavity, pelvic organs, and external genitalia.
Parasympathetic nerves consist mainly of long, lightly myelinated preganglionic fibers (type B) according to the Erlanger-Gasser classification. Ganglia are located directly in the walls of target organs (intramurally) or in their immediate vicinity. As a result, unmyelinated postganglionic fibers (type C) are extremely short. Signal irradiation occurs only at the organ itself, making the parasympathetic influence strictly local.
Physiological effects
The system exerts a global calming effect, promoting anabolic reactions (assimilation) and energy restoration:
- Cardiovascular system: myocardial excitability is reduced, heart rate and contractile force are decreased, and blood pressure falls.
- Respiration and thermoregulation: pulmonary ventilation volume and overall body temperature decrease.
- Metabolism: general metabolic rate drops. Insulin secretion increases, leading to a decrease in blood glucose levels and active deposition of intracellular glycogen.
- Digestion: secretory, motor, and absorptive functions of the gastrointestinal tract are simultaneously enhanced.
Important rule: the parasympathetic system does not innervate the smooth muscle of most blood vessels. The only exceptions are the vessels of the brain, salivary glands, mesentery, and genitals.
Synaptic transmission and regulation
Excitation transmission in the parasympathetic system occurs faster than in the sympathetic system. The main neurotransmitter at all stages is acetylcholine. The process of its release is triggered by the influx of calcium ions into the presynaptic terminal.
At the postsynaptic membrane of the organ, acetylcholine binds to muscarinic receptors (M1-Rs), which activates the enzyme guanylyl cyclase. It converts GTP into the secondary messenger — cGMP.
The effect of acetylcholine is always discrete. This is due to the abundance of the enzyme acetylcholinesterase in the postsynaptic cleft, which instantaneously breaks down the neurotransmitter.
Neurotransmitter release is tightly controlled by presynaptic regulation (feedback):
- Autoregulation: accumulated acetylcholine acts on its own presynaptic M2-Rs, inhibiting further exocytosis.
- Cross-inhibition: the sympathetic neurotransmitter (norepinephrine) can act on presynaptic $\alpha_2$-adrenergic receptors of parasympathetic terminals, also blocking acetylcholine release.
Briefly: answers to topical questions
Which muscarinic cholinergic receptor subtypes (M1, M2, M3) are located in various target organs?
Muscarinic cholinergic receptors have different localizations depending on the subtype.
- Subtype M1 is located in the stomach on enterochromaffin-like cells; also, in the parasympathetic transmission scheme, acetylcholine binds to M1 cholinergic receptors on the postsynaptic membrane.
- Subtype M2 is present in the heart and mediates the inhibitory influence of the parasympathetic nervous system; it is also found on the presynaptic membrane, where it participates in the autoregulation of acetylcholine release.
- Subtype M3 is the largest group: it is localized in ocular structures (sphincter pupillae, ciliary muscle), smooth muscle of internal organs (bronchi, stomach, intestines, biliary tract, urinary bladder, uterus), exocrine glands (bronchial, gastric, intestinal, salivary, lacrimal, nasopharyngeal, sweat; also gastric and pancreatic glands), and on non-innervated M3 cholinergic receptors of the vascular endothelium.
What is the mechanism of bradycardia development during vagus nerve stimulation at the ion channel level?
During vagal bradycardia, acetylcholine acts on cardiac M2 cholinergic receptors: M2 receptors inhibit adenylate cyclase via the Gi pathway and exert an inhibitory effect on the heart.
At the level of ionic processes for inhibitory synapses of the autonomic nervous system, sources indicate the following mechanism: inhibitory neurotransmitters, including acetylcholine, increase membrane permeability to $K^+$ and $Cl^-$ ions. $K^+$ exits the cell, and $Cl^-$ enters the cell along its concentration gradient. As a result, membrane hyperpolarization occurs, an inhibitory postsynaptic potential is formed, the excitation threshold increases, excitability decreases, and action potential propagation is blocked.
Through which autonomic ganglia do the parasympathetic fibers of the oculomotor, facial, and glossopharyngeal nerves pass?
Parasympathetic preganglionic fibers of the indicated cranial nerves head toward the following autonomic ganglia:
- Oculomotor nerve (III pair) — fibers pass to the ciliary ganglion (ganglion ciliare), from which postganglionic fibers extend to the sphincter pupillae and ciliary muscle.
- Facial nerve (VII pair) — fibers travel to the pterygopalatine ganglion (ganglion pterygopalatinum) and the submandibular ganglion.
- Glossopharyngeal nerve (IX pair) — fibers relay through the otic ganglion (ganglion oticum), providing innervation to the parotid salivary gland.
Sympathetic — "fight or flight" (ganglia close to the spinal cord, generalized response). Parasympathetic — "rest and digest" (ganglia right in the organ, focal response).
Class and exam questions
This is due to the enzymatic inactivation of the neurotransmitter. Acetylcholinesterase destroys parasympathetic acetylcholine much faster and more aggressively than MAO and COMT enzymes destroy sympathetic norepinephrine.
This is due to enzymatic inactivation. Acetylcholinesterase in synapses breaks down the parasympathetic neurotransmitter (acetylcholine) much faster and more powerfully than MAO and COMT enzymes break down sympathetic norepinephrine.
What is the essence of the phenomenon of acetylcholine overflow into the blood (according to V.P. Babkin)?
Normally, acetylcholine is broken down in the synapse. However, if cholinesterase is blocked (e.g., with eserine), the neurotransmitter enters the systemic circulation, causing generalized reactions: bradycardia, a drop in blood pressure, and inhibition of GI motility.
How does organ sensitivity change when parasympathetic nerves are damaged?
According to the Cannon-Rosenblueth law of denervation, structures deprived of innervation become hypersensitive to acetylcholine due to a sharp decrease in the concentration of the degrading enzyme (acetylcholinesterase) in the tissues.
What else to study on this topic
- Cannon and Rosenblueth's Law of Denervation
- Erlanger-Gasser Classification of Nerve Fibers
- Secondary Messengers (GC and cGMP) in Signal Transduction
- Interaction Between the ANS and the Endocrine System
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