A&p 201 Exam 3 Study Guide

Front 1

Difference in concentration gradients of ions across excitable cell membrane.

Back 1

Na+ is 12x higher on outside of cell; K+ is 40x higher on inside of cell.

Front 2

3 reasons why membrane potential (difference in charge) exists across a cell membrane.

Back 2

1. Na+/K+ pump is always exchanging 3 Na+ out of cell for 2 K+ entering cell (big use of energy); 2. Anions-negative proteins inside cell; 3. K+ diffuses out 50-100X faster than Na+ diffuses in.

Front 3

Difference b/w leakage channels and gated channels.

Back 3

Leakage: none-gated channels; passive/always open
Gated: active

Front 4

4 Types of Gated Channels

Back 4

; a) VOLTAGE GATED - open/close in response to membrance potential, b) CHEMICALLY GATED - open/close in response to chemical stimuli, cc) MECHANICALLY GATED - open/close in response to touch, pressure, vibration, d) LIGHT GATED - open-close in response to light

Front 5

2 Event of an Action Potential

Back 5

#1 - Incr Na+ permeability = 5000X (about 20,000 ions pass through membrane in that area) Reverses charge (outside/inside): Membrane is depolarized: "Firing" of action potential = "active"
#2 - Na+ gates close immediately after Na+ leakage; K+ voltage gates open and K+ permeability incr; membrane is "repolarized" = back to rest

Front 6

How ionic flow stimulates next adjacent area of membrance to fire an AP.

Back 6

PP#24-unmyelinated neuron &#25-myelinated neuron: has wave effect. Na+ ions leak thru open gates, cause membrane depolarization and diffuse to nearby membrane regions result in same effect to neighboring regions (all the way to end of neuron membrane). Neuron lined up fire, causing neurons next to them to fire, all the way down a line. After membranes reach threshold, an action potential 'fires', then membrane starts repolarization. Process repeats over and over as action potential moves down the membrane.

Front 7

What happens @ threshold

Back 7

Membrane potential t/b reached in order to trigger a action potential.

Front 8

"The all-or-none law"

Back 8

An action potential occurs at the same velocity/intensity, or it doesn't occur.

Front 9

Relative refractory period

Back 9

From potassium channel closing to return to resting membrane potential. AP can be fired, but stimulus w/b greater.

Front 10

Absolute refractory period

Back 10

From sodium channel opening to patassium channel closing: no AP can be fired during this time.

Front 11

Epimysium

Back 11

CT layer covers the entire muscle.

Front 12

Perimysium

Back 12

CT layer covers/surrounds fascicles inside the muscle.

Front 13

Endomysium

Back 13

CT layer surrounds individual muscle cells.

Front 14

Part of muscle cell @ histology level.
(KNOW PRINTED VIEW)

Back 14

SARCOPLASM: cytoplasm of muscle cell
SARCOLEMMA: plasma membrane of muscle cell
MITOCHONDRIA: to generate muscle cell ATP
MULTIPLE NUCLEI: to "control" this very big (=long) cell
SARCOPLASMIC RETICULUM: stores calium ions needed to effect concentration
T-TUBULES: tunnel-like infoldings to conduct action potential into each muscle cell
MYOFIBRILS: 100's lying parallel in muscle cell

Front 15

What happens during muscle contraction to:
A-Band
I-Band
Z-Lines
H-Zone
Bare Zone
M-Line
Sarcomere
Bare Zone
Titin
(SEE HANDOUT)

Back 15

A-Band: think filaments, stay same length
I-Band: gets smaller, may disappear (thin filament only)
Z-Lines: (define ends of sarcomeres): move closer together
H-Zone: disappears, it is the 'bare region', no overlap of filaments in resting muscle
Bare Zone: = H - zone and it disappears
M-Line: in middle of H-Zone
Sarcomere: basic functional unit of a muscle cell, gets shorter
Bare Zone: disappears
Titin: springy protein - to return muscle cell to normal resting length

Front 16

14 steps of how muscle shortens during contraction.

Back 16

1. Arrival of signal from nerve cell.
2. ACh is released from motor neuron into synaptic cleft
3. ACh binds to an ACh receptor protein on muscle fiber's motor end plate (in muscle cell membrane) causing ligand-gated ion channel to open & an (end plate potential) to form.
4. End-plate potential stimulates opening of Na+ voltage-gated ion channels causing an AP in the muscle fiber membrane.
5. AP moves along sarcolemma & down T-tubules
6. Active sites for myosin binding are exposed
7. AP moving down cause T-tubule stimulation resulting in #8
8. Sarcoplasmic reticulum release of Ca++ from terminal cisternae. Ca++ binds troponin-C: shape changes moving tropomyosin off actin.
9. Active sites for myosin binding on actin are exposed.
10. Cocked (activated) myosin heads from cross-bridges w/actin binding-sites
11. Attachment of myosin cross-bridges - heads pivot resulting in #12
12. Power stroke occurs: after movement of myosin heads, the ADP&P are released from the heads
13. Binding of new ATP to the 'open site' on myosin head breaks the cross-bridge
14. Myosin head hydrolyzes the new ATP and 're-cocks' for the next cycle

Front 17

G-actin

Back 17

single, globular units of actin

Front 18

F-actin

Back 18

linear strand (like a pearl necklace) of G-actin units

Front 19

Tropomyocin

Back 19

thread-like protein rests upon & blocks surface of actin. Each one covers 7 sites of active ("binding") actin. Blocks binding site to myosin.

Front 20

Troponin

Back 20

Complex of three globular proteins. Each has affinity for: Actin, Tropomyocin or Calcium

Front 21

Structure of Myosin

Back 21

Made of 2 identical subunits & 2 bulbous heads (cross bridges). Heads connect to a tail at the hinge. Myosin binds to actin, energy in myosin head causes head to tilt, pulling action toward center of A-band (=shorter) sarcomere.