How are action potentials propagated How are action potentials propagated? Oct 30 Nov 1: Happy Halloween Last stuff for Lecture Exam #3 Friday In terms of Na+ and K+, what is the cause of an action potential? What happens to the membrane potential when an action potential is created? Why does a depolarized membrane rapidly return to its hyperpolarized state? Compare and contrast action potential propagation along myelinated and unmyelinated axons. REVIEW of skeletal muscle function.

Rule #2 of Zombie Encounters is to “double tap”.

When excitable cells (neurons and myofibers) are at rest they have lots of potassium on the inside and lots of sodium outside of the cell. They exhibit excitability when Na+ and/or K+ suddenly move across the plasma membrane through special channels that open for this specific purpose! These channels continue this process along the length of the membrane.

An action potential occurs when a depolarization is initiated and propagates itself down the length of a neuron or muscle cell. STEPS? Step One: Something initiates local depolarization (generator potential) -Damage -Ligand-gated ion channels are often opened by acetylcholine or other neurotransmitter compounds (ligand): I.E. the neuromuscular junction -Stretch/Mechano receptors (ion channels): Cells in the ear work this way -Leaking ions passing through gap junctions: Cardiac cells work this way Step Two: Voltage gated channels detect a local change in membrane potential that was created (step 1) causing individual VG-Na+ channels to become open for only a few microseconds (Na+), before they close again! Step Three: Other neighboring voltage gated Na+ channels open (see step 2) further along the membrane due to local change in voltage! These channels also open, then close. Step Four: The self-propagating wave moves away in all directions from the origin, and an action potential is formed!

Could you discuss what happens during the 7 steps shown above? What causes hyperpolarization above at step #6? The action potential on an axon or skeletal myofiber are very similar, AP on a cardiac myocyte is very dissimilar! V.I.P.

Action Potentials are: 1)All-or-none, 2)Self-propagatory, 3)Irreversible, and 4)Non-decremental! Membranes normally exist at the Resting Membrane Potential: 1) Sub-threshold stimulus (generator potential) leading up to threshold. 2and 3) Depolarization Occurs when threshold of local voltage gated channels causes them to open! VIP!! Non excitable cells lack voltage gated channels! 4) Maximum depolarization is reached then voltage gated Na+ channels start to close, then K+-Channel start to open and the membrane potential moves back in the negative direction. 5) Abs. Refract. Period: Repolarization is occurring, the Na+ channels are closed and they cannot be reopened! 6) Relative Refractory Period: unusually strong stimuli needed to depolarize the membrane. (why?) 7) Original membrane potential is re-established and cell waits to repeat action.

Once initiated, action potentials can be transmitted slowly or rapidly: 1) Slowly: regular conduction of AP along unmyelinated neurons 2) Very Rapidly: saltatory (jumping) conduction of AP between Nodes of Ranvier (exposed membrane) on myelinated neurons!

AP propagation along an unmyelinated neuron: axons normally carry the AP away from cell body to the next cell! If the stimulus occurs artificially in the middle of an axon, (injury) the AP can travel both ways!

The myelin sheath is created by non-excitable cells called: Oligodendrites in the central nervous system Schwann Cells in the peripheral nervous system The exposed gaps between cells are called Nodes of Ranvier

What is an “excitable” membrane? Can you describe this in your own words? How do epithelial cells differ from neurons and myofibers? What is voltage? What is a membrane potential?

How does a membrane depolarization cause calcium to enter a muscle cell? The Sequence of Events: 1) Change membrane potential (voltage) From Very Negative to Positive Charge! 2) Ion channel proteins in membrane change shape when a certain voltage is detected. 3) Channels for Na+ open and Na+ enters cell 4) Channels for calcium transport change shape and become wide-open! 5) Calcium enters sarcoplasm (cytosol) from: sarcoplasmic reticulum and t-tubules 6) Ca++ diffuses to troponin and tropomyosin is removed! 7) Myosin Head can find binding site on actin! 8) Myosin-ATPase: Power strokes begin! 9) Strokes continue until Ca++ or ATP is removed! ….Recovery with membrane voltage repolarization…..

Depolarization opens Ca++ channels>>Ca++ enters/diffuses/binds troponin>>TropoMYOSIN is pulled off>> Myosin head can bind actin.

How does the cortex of your brain send a message to your skeletal muscle cells that causes them to contract? Nerve cell axon ending meets myofiber at a structure called the: Motor End Plate or Synapse or Neuromuscular Junction Three names for the same basic thing Synaptic cleft: space between axon and myofiber Axon contains/releases synaptic vesicles: Vesicle contain neurotransmitter (acetylcholine or ACH) ACH opens Na+ channels that cause depolarization What limits duration of depolarization? 1) Voltage gated channels (Na+ and Ca++) only stay open for a few microseconds, then they automatically close 2) Acetylcholinesterase degrades ACH ACH-ase inhibitors are used for chemical warfare, causing a fatal seizure (contraction)! 3) Sodium and calcium (Ca++) are rapidly pumped out

Depolarization of the target cell occurs when the ACH in a vesicle is released (exocytosis), diffuses across synapse, and binds/open its receptor (a Ligand Gated-Na+ Channel)

End Plate “Potential”: One exocytosis may not release enough ACH to open enough ligand-gated channels to create enough depolarization to cause enough depolarization to open the voltage gated channels.

Review of structural organization

How does the orientation of actin and myosin heads at the start of contraction effect potential force generation?

Review: Muscles/Myofibers/Sarcomeres have an ideal length that gives them the best contractile performance for a given stimulation. This is called the Length-Tension Relationship