Ims: Zimmerman Block 1 - End

Front 1

In what types of cells would having a long undershoot be helpful?

Back 1

Cells needing to perform rhythmic or pacemaking functions.

Front 2

What does the AP of cardiac cells look like? Why?

Back 2

Plateau - has tons of Ca2+ channels, makes Vm go up, also has lots of delayed rectifier K+ chanels, so Vm closer to Ek .

Front 3

How many APs per heart beat?

Back 3

One

Front 4

How does the AP in the atrium differ from the AP in the ventricles? Why?

Back 4

Smaller plateau; doesn't need to generate as much force

Front 5

Describe how the SA node produces a pacemaker potential.

Back 5

1. Membrane starts out negative bc of large number of open K+ channels

2. This hyperpol induces opening of nonselective cation channels, resulting in influx of cations (Ih), which cause membrane to depol

3. Depol opens Ca2+ selective channels, producing Ca2+ AP

4. This depol causes delayed opening of more K+, sending membrane more negative, closing Ca2+ channels

5. This hyperpol reactivates nonsel cation channels (Ih) and deactivates delayed rectifier K+ ch

Front 6

What is the advantage to having the SA node generate pacemaker potentials?

Back 6

Doesn't require neural input!

Front 7

How does cAMP interact with hyperpolarization activated nuleotide regulated channels in the SA node? How is this process affected by norepi?

Back 7

HCN (nonsel cation channel) has binding site for cAMP/cGMP, when these bind, channels open at a less negative Vm and at at a quicker rate.

Norepi activates adrenergic recptors, adenylcyclase makes cAMP, makes channels open faster, get AP's sooner, get faster heart rate

Front 8

What ions do HCN channels allow to pass?

Back 8

Non-sel cation channel

Front 9

What comprises thin filaments in muscle?

Back 9

Actin

Front 10

What comprises thick filaments in muscle?

Back 10

Myosin and myosin heads

Front 11

What does the sliding filament theory state? What does this require?

Back 11

Filaments slide toward each other during contraction, causing the sarcomere to shorten

Requires optimal length such that myosin heads can reach actin binding site (requires optimal overlap of thin and thick fils)

Front 12

Describe how myosin heads cause contractions.

Back 12

1. The myosin head, bound with ADP and P, binds to the actin filament in the presence of Ca2+.

2. The binding of the myosin head to actin causes release of P, and then ADP, and a resulting conformational change of the head that pulls the actin filament (the "power stroke").

3. The myosin remains bound to the actin filament until an ATP molecule binds to the myosin head. ATP binding causes release of myosin from actin.

4. The myosin head hydrolyzes the ATP to ADP and P, causing the myosin head to return to its original "cocked" conformation, ready to bind actin again.

Front 13

Describe calcium-induced calcium release in muscles.

Back 13

AP travels along T-tubles, Calcium binds calcium receptor on SR (RYANADINE RECEPTOR), which opens Calcium channels, which releases more calcium.

ATP-driven pumps bring Calcium back in

Minimal Ca2+ so no great effect on Vm

Front 14

How is actin affected by calcium?

Back 14

Actin has tropinin and topomyosin

Tropomyosin blocks myosin binding site

When calcium binds troponin, tropomyosin moves out of the way and lets myosin form x-bridge

Front 15

What role does ATP play in muscle contractions?

Back 15

ATP binds myosin head, causing head to relase actin, ATP hydrolyzed, recocks myosin head

Also fuels Ca2+ pump in SR to move calcium back into SR

Front 16

Contrast isometric with isotonic.

Back 16

Isometric (same distance): muscle tense but not moving anything (ex: pushing against wall)

Isotonic (same weight): can pick up lighter things easier than heavy loads, requires more cross bridges to balance load

Front 17

What is phosphocreatine used for in muscle?

Back 17

Back up for ATP

Front 18

Why is there a delay in muscle contraction after AP?

Back 18

Delay bc calcium needs to be released, x-bridges need to be formed

Front 19

How can you adjust AP's to get a larger twicth?

Back 19

TETANUS! Sum up subsequent AP's; tension doesn't have a refractory period

This is the normal mode of action in muscle

Front 20

What is a series elastic component? How does it work?

Back 20

When muscle contracts, begins stretching tendon before get movement. Requires additional AP's. Adds delay, but allows smooth movement. This is series elastic component.

Front 21

What is the parallel elastic component? When is it used?

Back 21

Only comes into play when you have over-stretching of muscle.

Front 22

What is a motor unit comprised of? How are motor unit number and load size related?

Back 22

Motor unit: motor neuron and all connecting muscle fibers
Big loads require more x-bridges, and more motor units contributing

Front 23

What is spatial summation?

Back 23

Get more muscles involved to lift a heavy load

Front 24

What are intrfusal fibers?

Back 24

MUSCLE SPINDLES: are merely sensory; tell you how contracted muscle is; as muscle contracts, spindles contract (due to sensation, not muscle contraction)

Front 25

What is the Golgi Tendon Organ?

Back 25

Bone nerve endings that stretch when you overstretch muscle

Front 26

Does skeletal muscle have gap junctions?

Back 26

NO

Front 27

What allows smooth muscle cells to coordinate peristalsis?

Back 27

Gap jns

Front 28

How do smooth muscle contractions differ from skeletal muscle contractions?

Back 28

Slower turn on/off than skeletal muscle

Calcium binds CALMODULIN which interacts with MYOSIN LIGHT CHAIN KINASE, Pi's myosin head, binds actin

Now need phosphatase to remove Pi from myosin

Most of calcium come from extracell; some from SR. Thus most Ca++ needs to be pumped out of cell

Front 29

How does cardiac muscle contraction compare with skeletal muscle? With smooth muscle?

Back 29

Same but has gap jns (allows synchronous behavior)

Lots of ca2+ from extracell

FASTER than smooth, SLOWER than skel

Front 30

Describe synaptic transmission in cardiac cells. Use ions.

Back 30

AP travels, depol

Na+ ch opens

Na+ enters, repels K+ through gap jns

K+ in next cell, goes to membrane (capacitor), depol, Na+ ch open

Etc. etc.

Front 31

Describe synaptic transmission in the neuromuscular junction.

Back 31

AP travels, Ca2+ channels open

Ca2+ binds vesicles, fuse membrane, release contents (Ach)

ACh binds ligand-gated channels, opens them

If non-sel cation ch, Na+ in

Depol membrane, voltage gated ch's open, more Na+ in

Front 32

What is the reversal potential for a non-selective cation channel?

Back 32

~0

Front 33

What kind of potential does Ach cause when it binds post synaptic receptors?

Back 33

Local potential, but get so many local potentials from ACh, you reach threshold: KNOWN AS END PLATE POTENTIAL AKA EXCITATORY POST SYNAPTIC POTENTIAL

Front 34

When wouldn't you get an AP in muscle? Think in terms of ACh.

Back 34

1) ACh receptors out of commission (Autoimmune dz, eg., myacenia gravis)

- ACh receptors under attack; eg, snake venom blocks it

-Problem in manufacture of ACh

Front 35

What NT's allow for an excitatory post synaptic potential? What does an EPSP cause?

Back 35

ACh, Glutamate

Opens non-sel cation channels

Front 36

What NT's allow for an inhibitory post synaptic potential? What does an IPSP cause?

Back 36

GABA

Cl-, K+ channels open

Front 37

What is the initial segment of a neuron? How does it work?

Back 37

Axon hillock

High resistance, lots of Na+ channels and delayed rectifiers, generates AP

Front 38

How does myelin affect the membrane's ability to act as a capacitor?

Back 38

Fewer charges stored on a thick insulator, which blocks exit routes, decreasing leakage from cell, speeds up conduction

Front 39

How does presynaptic inhibition work?

Back 39

A synapses onto B, but synapses subthreshold. So you get a slight depolarization in Cell B.

This results in ACCOMMODATION: deactivates Na+ channels, which can prevent AP propagation in Cell B, so Cell C doesn't get excited

Longer A dribbles on B, the more Na+ channels that will be deactivated.