Chapter 11: Efferent Division

Autonomic division

Controls smooth and cardiac muscle, glands, and adipose tissue (involuntary)

Somatic motor division

Controls skeletal muscle (mostly voluntary)

CNS structures that regulate autonomic function

Hypothalamus, pons, and medulla regulate autonomic reflexes (e.g., blood pressure, breathing, water balance)

antagonistic control in the ANS (Autonomic Nervous System)

• Sympathetic stimulation = excitatory

• Parasympathetic stimulation = inhibitory (and vice versa)
  

• Example:

  • Sympathetic → ↑ heart rate

  • Parasympathetic → ↓ heart rate

anatomy of autonomic pathways

• Two-neuron chain:

  • Preganglionic neuron: CNS → ganglion

  • Postganglionic neuron: ganglion → effector

• Divergence: One preganglionic fiber can synapse on many postganglionic neurons

sympathetic pathway

Thoracolumbar spinal cord

Parasympathetic pathway

• Brainstem and sacral spinal cord (e.g., vagus nerve contains ~75% of parasympathetic fibers)

Preganglionic

• (both)

  • ACh → nAChR

Sympathetic postganglionic

NE → adrenergic receptors (α, β)

Parasympathetic postganglionic

ACh → mAChR

α1 receptor

NE > E; activates phospholipase C (↑ IP₃, DAG → ↑ Ca²⁺)

β1 receptor

NE = E; activates cAMP

β2 pathway

E > NE; activates cAMP

muscarinic receptors (mAChR)

• Found on parasympathetic targets

• G protein–coupled

• Use second messenger cascades

• Have multiple subtypes

neuroeffector junction

• Synapse between postganglionic neuron and target cell

• Varicosities release neurotransmitter into interstitial fluid, not a synaptic cleft

NE release and removal

1. AP → varicosity

2. Ca²⁺ influx

3. Exocytosis of NE

4. NE binds adrenergic receptor

5. NE removed by diffusion, reuptake, or MAO degradation

adrenal medulla's role

• Neuroendocrine tissue that releases epinephrine into the bloodstream

• Functions as part of the sympathetic nervous system

β-blockers

(e.g., propranolol): block β-adrenergic receptors

MAO inhibitors

(e.g., selegiline): prevent NE breakdown

Cocaine

blocks NE reuptake → toxic sympathetic overactivation

Organophosphates

(AChE inhibitors): overstimulate AChRs

Nicotinic (MTWHF) poisoning

sign of organophosphate poisoning

• Mydriasis, Tachycardia, Weakness, Hypertension, Fasciculations

Muscarinic (DUMBELS) poisoning

type of organophosphate poisoning

Diarrhea, Urination, Miosis, Bronchorrhea, Emesis, Lacrimation, Salivation

dysautonomia

Dysfunction of ANS, often related to diabetes, MSA, or Parkinson’s

somatic motor pathway

• Single myelinated neuron from CNS to skeletal muscle

• Always excitatory

• Neurotransmitter: ACh

• Receptor: nAChR (Nm subtype)

neuromuscular junction (NMJ)

• Presynaptic terminal (vesicles + mitochondria)

• Synaptic cleft

• Motor end plate on muscle (high [nAChRs])

• Enzyme: Acetylcholinesterase (AChE)

neurotransmitter release at the NMJ

1. AP → Ca²⁺ channels open

2. ACh vesicles released

3. ACh binds nAChR

4. Na⁺ enters, K⁺ exits → depolarization

5. AP in muscle → contraction

6. ACh broken down by AChE

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myasthenia gravis

• Autoimmune disease that destroys ACh receptors at NMJ

• Causes muscle weakness (worse with activity)

• Symptoms: drooping eyelids, difficulty speaking, swallowing, breathing