Membrane Potentials and Action Potentials

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Membrane Potentials andAction Potentials
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• Voltage-Gated Sodium ChannelActivation and
  Inactivation of the Channel

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Roles of Other Ions During the Action Potential

• Impairment Negatively Charged Ions (Anions)
  Inside the Nerve Axon
• Calcium Ions. Ca-Na channels (slow channels)
• Increased Permeability of the Sodium Channels
  When There Is a Deficit of Calcium Ions.

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Initiation of the Action Potential

• A Positive-Feedback Vicious Cycle Opens the
  Sodium Channels.
• Threshold for Initiation of the Action Potential.

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Propagation of the Action PotentialDirection of
Propagation. All-or-Nothing Principle.
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Re-establishing Sodium and Potassium Ionic
Gradients After Action Potentials Are
CompletedImportance of Energy Metabolism

• That is, as the internal sodium concentration
  rises from 10 to 20 mEq/L, the activity of the
  pump does not merely double but increases about
  eightfold.

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Plateau in Some Action Potentials First, in
heart muscle, two types of channels (1) the
usualvoltage-activated sodium channels, called
fast channels, and (2) voltage-activated
calcium-sodium channels, which are slow to open
and therefore are called slow channels. A second
factor that may be partly responsible for the
plateau is that the voltage-gated potassium
channels are slower than usual to open,
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Special Characteristics of Signal Transmission in
Nerve Trunks

• Myelinated and Unmyelinated Nerve Fibers.
• Saltatory Conduction in Myelinated Fibers from
  Node to Node.

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• Saltatory conduction is of value for two reasons.
  First, by causing the depolarization process to
  jump long intervals along the axis of the nerve
  fiber, this mechanism increases the velocity of
  nerve transmission in myelinated fibers as much
  as 5- to 50-fold.
• Second, saltatory conduction conserves energy for
  the axon because only the nodes depolarize,
  allowing perhaps 100 times less loss of ions than
  would otherwise be necessary, and therefore
  requiring little metabolism for reestablishing
  the sodium and potassium concentration
  differences across the membrane after a series of
  nerve impulses.
• 50- fold decrease in membrane capacitance allow
  repolarization to occur with very little transfer
  of ions.

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• Contraction of Skeletal Muscle

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Physiologic Anatomy of Skeletal Muscle

• The sarcolemma is the cell membrane of the muscle
  fiber
• Myofibrils Actin and Myosin Filaments.
• The thick filaments in the diagrams are myosin,
  and the thin filaments are actin.
• The light bands contain only actin filaments and
  are called I bands because they are isotropic to
  polarized light.

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• The dark bands contain myosin filaments, as well
  as the ends of the actin filaments where they
  overlap the myosin, and are called A bands
  because they are anisotropic to polarized light.
• cross-bridges.
• Z disc.
• The portion of the myofibril (or of the whole
  muscle fiber) that lies between two successive Z
  discs is called a sarcomere.

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• Sarcoplasm The spaces between the myofibrils are
  filled with intracellular fluid called sarcoplasm
• Sarcoplasmic Reticulum.

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General Mechanism of MuscleContraction

• 1. An action potential travels along a motor
  nerve to its endings on muscle fibers.
• 2. acetylcholine.
• 3. acetylcholinegated channels
• 4. large quantities of sodium ions
• This initiates an action potential at the
  membrane.

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Synaptic vesicle exocytosis
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• 6. Release large quantities of calcium
• 7. The calcium ions initiate attractive
• 8. the calcium ions are pumped back into the
  sarcoplasmic

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Molecular Mechanism of Muscle Contraction

• Myosin Filament.
• ATPase Activity of the Myosin Head
• Actin Filament.

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Cross Bridge
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• 1. Before contraction begins, the heads of the
  crossbridges bind with ATP. The ATPase activity
  of the myosin head immediately cleaves the ATP
  but leaves the cleavage products, ADP plus
  phosphate ion, bound to the head.
• 2. When the troponin-tropomyosin complex binds
  with calcium ions, active sites on the actin
  filament are uncovered, and the myosin heads then
  bind with these
• 3. The bond between the head of the cross-bridge
  and the active site of the actin filament causes
  a conformational change in the head, prompting
  the head to tilt toward the arm of the
  cross-bridge. This provides the power stroke for
  pulling the actin filament
• 4. Once the head of the cross-bridge tilts, this
  allows release of the ADP and phosphate ion that
  were previously attached to the head. At the site
  of release of the ADP, a new molecule of ATP
  binds. This binding of new ATP causes detachment
  of the head from the actin.

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• 5. After the head has detached from the actin,
  the new molecule of ATP is cleaved to begin the
  next cycle, leading to a new power stroke.
• 6. When the cocked head (with its stored energy
  derived from the cleaved ATP) binds with a new
  active site on the actin filament, it becomes
  uncocked and once again provides a new power
  stroke.

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Interaction of One Myosin Filament, Two Actin
Filaments, and Calcium Ions to Cause Contraction
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• Excitation of Skeletal Muscle Neuromuscular
  Transmission and Excitation-Contraction Coupling

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