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Somatic and Autonomic Nervous System Physiology

Somatic Nervous System

  • Leaky K extsuperscript{+} Channels

    • Always open, maintaining a gradient.
    • K extsuperscript{+} is intracellular, Na extsuperscript{+} extracellular; ions move down their concentration gradient.

  • Signal Initiation

    1. Signal from the Peripheral Nervous System (PNS).
    2. Opening of Na extsuperscript{+} channels (graded potentials).
    3. Graded potentials sum up leading to an action potential (AP).

  • Action Potential Generation

    1. Threshold reaches -55 mV.
    2. Voltage-gated Na extsuperscript{+} channels open, Na extsuperscript{+} rushes in.
    3. Membrane depolarizes to +30 mV.
    4. At +30 mV, inactivation gate of Na extsuperscript{+} channels closes, while activation gate remains open (absolute refractory period).
    5. Voltage-gated K extsuperscript{+} channels open concurrently.
    6. Membrane hyperpolarizes to -70 mV (relative refractory period).

  • Role of Calcium Ions (Ca extsuperscript{2+})

    1. Action Potential (AP) causes voltage-gated Ca extsuperscript{2+} channels to open.
    2. Ca extsuperscript{2+} influx causes vesicles to fuse with the membrane.
    3. Glutamate is released via exocytosis.
    4. Glutamate binds to lower neuron's Na extsuperscript{+} channels (steps 3-12 repeat).

  • Acetylcholine (ACh) Release

    1. ACh is released through exocytosis.
    2. ACh binds to nicotinic ACh receptors.
    3. ACh is then hydrolyzed by acetylcholinesterase (AChE).
    4. AChE recycles ACh into the cell with the help of MG (magnesium).
    5. Nicotinic ACh receptor is a ligand-gated Na extsuperscript{+} channel.

  • Propagation of Action Potential

    1. AP from Na extsuperscript{+} influx travels down the T-tubule.
    2. Dihydropyridine (DHP) receptor on T-tubule reacts by opening Ryanodine (RyR) receptor.
    3. RyR releases Ca extsuperscript{2+} from sarcoplasmic reticulum (SR).

  • Muscle Contraction Mechanism

    1. Ca extsuperscript{2+} binds to troponin.
    2. Troponin releases tropomyosin from covering actin.
    3. Myosin heads become erect, attaching to actin filaments.
    4. Power stroke occurs leading to muscle contraction.
    5. Phosphate (P) on myosin releases, followed by ADP.
    6. New ATP binds to myosin head.
    7. SERCA pump reabsorbs Ca extsuperscript{2+} back into SR.
    8. Decrease in intracellular Ca extsuperscript{2+} levels causes Ca extsuperscript{2+} to unbind from troponin.
    9. Tropomyosin covers actin again.
    10. Myosin returns to a relaxed state.

Autonomic Nervous System

  • Autonomic (Smooth Muscle) Physiology
Parasympathetic Pathway
  1. Leaky K extsuperscript{+} channels always open (sets gradient) leading to a resting state.
  2. Signal from Central Nervous System (CNS) (cervical or sacral).
  3. Opening of Na extsuperscript{+} channels results in graded potentials.
  4. Sum of graded potentials leads to action potential at -55 mV.
  5. Voltage-gated Na extsuperscript{+} channels open, Na extsuperscript{+} influx occurs.
  6. Membrane depolarizes to +30 mV.
  7. At +30 mV, Na extsuperscript{+} channels inactivate, while activation gates remain open (absolute refractory period).
  8. Voltage-gated K extsuperscript{+} channels subsequently open.
  9. Membrane hyperpolarizes to -70 mV (relative refractory period).
  10. AP causes voltage-gated Ca extsuperscript{2+} channels to open.
  11. Vesicles fuse with membrane and release ACh through exocytosis.
  12. ACh binds to muscarinic receptor Na extsuperscript{+} channels, generating a new AP in the target cell.
  13. Ca extsuperscript{2+} enters the cell and binds to Calmodulin complex.
  14. Myosin light chain kinase (MLCK) phosphorylates myosin light chains leading to muscle contraction.
Sympathetic Pathway
  1. Similar initial steps to the parasympathetic pathway (steps 1-15).
  2. Norepinephrine is released through exocytosis.
  3. Norepinephrine can bind to alpha (α1, α2) and beta (β) adrenergic receptors.
  4. Adrenal glands release epinephrine into the bloodstream.
  5. Epinephrine binds to beta-2 (β2) receptors.
  6. Binding of epinephrine decreases MLCK activity, causing relaxation of smooth muscles.
  7. Reduced Ca extsuperscript{2+} levels lead to Ca extsuperscript{2+} unbinding from the Calmodulin complex.
  8. Myosin light chains undergo dephosphorylation, leading to relaxation as myosin unbinds from actin.

Autonomic (Cardiac Muscle) Physiology

  • Similar Mechanism to Skeletal Muscle
  1. Leaky K extsuperscript{+} channels always open.
  2. Signal from CNS (cervical or sacral).
  3. Opening of voltage-gated Na extsuperscript{+} channels results in Na extsuperscript{+} influx.
  4. Graded potentials lead to an action potential at -55 mV.
  5. Na extsuperscript{+} channels fully open causes membrane depolarization to +30 mV.
  6. Na extsuperscript{+} channels then inactivate at +30 mV (absolute refractory).
  7. Voltage-gated K extsuperscript{+} channels activate.
  8. Membrane hyperpolarizes to -70 mV (relative refractory).
  9. AP causes voltage-gated Ca extsuperscript{2+} channels to open.
  10. Vesicles fuse and release ACh (exocytosis) activating muscle contraction and relaxation pathways similar to skeletal muscle.
  • Final Steps Include:
    • ACh binds to muscarinic Na extsuperscript{+} channels, causing potential changes in cardiac cells.
    • SERCA pumps return Ca extsuperscript{2+} to the SR.
    • Decreased Ca extsuperscript{2+} levels promote relaxation: Ca extsuperscript{2+} unbinding from troponin, tropomyosin covers actin, myosin returns to a relaxed state.