Notes on Autonomic and Somatic Nervous Systems
Autonomic and Somatic Nervous Systems
Autonomic Nervous System (ANS)
- Functions: Regulates activity in smooth muscle, cardiac muscle, and glands (visceral organs).
- Roles: Increases (Excitation) or decreases (Inhibition) ongoing activities.
- Branches:
- Sympathetic: Prepares body for emergencies (Fight or Flight).
- Parasympathetic: Conserves and restores energy (Rest and Digest).
- Enteric: Discussed in digestive system (Chapter 21).
- Dual Innervation: Most organs receive input from both sympathetic and parasympathetic systems.
- Pathway Composition: Comprised of two neurons - preganglionic and postganglionic.
Parasympathetic Division
- Craniosacral Division: Preganglionic neurons exit the CNS from the brain stem and sacral spinal cord.
- Terminal Ganglia: Preganglionic fibers synapse close to or at the target organs.
- Key Nerves:
- Oculomotor (III): Influences ciliary muscle for eye accommodation.
- Facial (VII): Innervates glands (tear, saliva).
- Glossopharyngeal (IX): Innervates salivary glands through otic ganglion.
- Vagus (X): Major nerve that innervates the thoracic and abdominal organs.
- Sacral Nerves: Innervate lower parts of large intestine, rectum, urinary, and reproductive organs.
Sympathetic Division
- Thoracolumbar Division: Preganglionic neurons located in the thoracic and lumbar regions (T1-L2).
- Ganglia: Includes paravertebral (sympathetic chain) and collateral (prevertebral) ganglia.
- Paravertebral Ganglia: Interconnected ganglia alongside the spinal cord.
- Collateral Ganglia: Splanchnic nerves synapse here impacting digestive, urinary, reproductive organs.
- Adrenal Medulla: Releases epinephrine and norepinephrine, extending the sympathetic response duration.
Neuroeffector Junction
- Definition: Synapse between autonomic postganglionic neurons and visceral effectors.
- Mechanism: Uses varicosities; neurotransmitters diffuse across the synapse to bind with receptors.
- Signal Transmission Process:
- Action potentials trigger Ca²⁺ influx at varicosities.
- Ca²⁺ stimulates neurotransmitter release.
- Neurotransmitter binding activates G proteins leading to excitation or inhibition.
Types of Neurotransmitters and Receptors
Cholinergic
- Neurotransmitter: Acetylcholine (ACh) used by all preganglionic neurons, most parasympathetic postganglionic, and some sympathetic postganglionic (e.g., sweat glands).
- Receptors:
- Nicotinic: Located at neuromuscular junctions and dendrites of autonomic neurons.
- Muscarinic: Found in smooth muscle and glands.
Adrenergic
- Neurotransmitters: Norepinephrine and Epinephrine, primarily released by the sympathetic system.
- Receptor Types:
- Alpha (α): Found in most sympathetic target tissues; promotes excitatory effects.
- Beta (β): Has multiple subtypes affecting various tissues with excitatory or inhibitory outcomes.
Autonomic Effects
- Sympathetic Stimuli: Increases heart rate, vasoconstriction, inhibits digestive functions, promotes glucose release, and prepares the body for emergencies.
- Parasympathetic Stimuli: Decreases heart rate, promotes digestion (SLUDD - Salivation, Lacrimation, Urination, Digestion, Defecation), and conserves energy.
- Balancing Activity: Homeostasis maintained by autonomic tone, dependent on hypothalamic regulation.
Somatic Nervous System (SNS)
- Regulation: Governs voluntary control of skeletal muscle.
- Structure: Composed of a single somatic motor neuron connecting directly with skeletal muscle fibers.
Neuromuscular Junction (NMJ)
- Components: Synaptic end bulb releases ACh; the motor end plate has receptors that cause excitatory effects.
Signal Transduction at NMJ
- Process:
- Action potential arrives, opening voltage-gated Ca²⁺ channels.
- Release of ACh triggering muscle action potential through Na⁺ influx.
Disturbances in NMJ Function
- Botulinum toxin: Blocks ACh release, can cause paralysis.
- α-latrotoxin: Leads to excessive ACh release, potentially causing respiratory failure.
- Curare: Blocks ACh receptors, used during surgery.
- Organophosphates: Inhibit acetylcholinesterase, prolonging ACh effects.