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A&P > exam 3 > Flashcards

exam 3 Flashcards

1
Q

action potential

A

Suprathreshold and the all or none principle

Doesnt require atp it uses diffusion

All leak channels stay open, Na+/K+ pump continues working

threshold reached

depolarization phase, voltage gated Na+ channels of trigger zone open

peak phase

repolarization phase

hyperpolarization phase

afterhyperpolarization phase

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2
Q

Suprathreshold and the all or none principle of action potential

A

Doesn’t matter if you barely got to the threshold, you got there

all responses are alike

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3
Q

All leak channels stay open, Na+/K+ pump continues working of action potential

A

not permeable to sodium

at stimulus noting changes on axon until it gets to threshold

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4
Q

threshold reached of action potential

A

Voltage channels achieve threshold of around -65

Opens voltage gated sodium channels which uses diffusion (passive)

The inside is relatively positive for a very brief moment

The insides still has more potassium than sodium

You can’t flip the gradient

Diffusion will just slow down

sodium channels open first

once close to peak potassium channels will open

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5
Q

depolarization phase, voltage gated Na+ channels of trigger zone open of action potential

A

Big upswing

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6
Q

peak phase of action potential

A

voltage gated K+ channels open

Na+ channels inactivated

sodium channels

gate slides into bottom of channel

cant be opened (unlike a closed channel)

absolute refractory period

Sodium channels and activated

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7
Q

why do channels inactivate

A

Each action potential is individualized

has to go from the beginning to the end before starting again

Can’t have summation

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8
Q

relative refractory period

A

Respond if have two

Relatively larger stimulus to be able to respond

Not at a normal resting potential

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9
Q

repolarization phase of action potential

A

reduced influx Na+

Potassium exiting by moving with the gradient

The inside goes back to negative

voltage gated K+ channels remain open

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10
Q

Hyperpolarization phase Of action potential

A

voltage gated K+ channels remain open

nactivation gate of voltage gated Na+ channels opens

sodium channels become closed instead of inactivated

relative refractory period

goes below resting for a little bit

Potassium leak channel gets carried away and stays open for a little bit

Gets put back inside through potassium pump against gradient

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11
Q

After hyperpolarization phase

A

voltage gated K+ channels close

membrane potential returns to resting value

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12
Q

look at picture for excitable cells

A

https://knowt.com/flashcards/1e72a942-e4f5-4922-9059-197ef4898d58?isNew=true

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13
Q

action potential propogation

A

self generating

like positive feedback

snowball

creates more action potentials

wat to make enough to go all the way from trigger zone to axon terminal

ions diffuse away from point of entry

previous segment is inactivated (absolute refractory period)

positive feedback

influence of axon diameter

influence of myelin`

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14
Q

positive feedback - action potential propagation

A

sodium will diffuse in both directions

from +30 axon to the -70 axon to make the -70 depolarize and reach threshold

only goes forward

sodium channels where the signal was just at are inactivated

absolute refractory period

don’t generate any signal in proceeding signal, just forward

that is why peak is so high

threshold: -55

resting: -70

middle: -30

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15
Q

influence of axon diameter- action potential propogation

A

drinking straw

wider is easier

narrow: more friction and resistance

axon

narrow: sodium ions have more contact with cell membrane of axon- more friction, resistance, and collisions

wider: just travel down middle

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16
Q

influence of myelin - action potential propogation

A

oligodendrocytes or schwann cells

oligodendrocytes: cell body, several branching structures, central

schwann cells- axon like we know, peripheral

covers/insulates sections- its fatty- not going to let ions out, cant travel through

nodes of ranvier

little gaps- ions can leak out here

saltatory conduction

signal hops or jumps from node to node

doesn’t look continuous

sodium ions diffuse

if diffuse enough

diffuse under myelin

cant leak out

reach potential

don’t have to generate action potentials

just reach threshold by diffusion

may lose some ions but just need enough to reach threshold

not on brain or spinal cord

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17
Q

Axon terminals

A

chemical synapses- always have space, requires energy: make neurotransmitter, release the proteins

electrical synapses

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18
Q

chemical synapses of axon terminals

A

voltage-gated calcium channels

vesicles maintaining neurotransmitter

exocytosis

ligand gated ion channels

fate of neurotransmitters

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19
Q

vesicles maintaining neurotransmitter of chemical synapses of axon terminals

A

spherical sac

contains protein (neurotransmitter)

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20
Q

exocytosis of chemical synapses of axon terminals

A

terminal end manufactured protein

vesicle migrate to surface and fuse with all membrane

what is inside cell moved out (exocytosis)

golgi apparatus packaging neurotransmitter into vesicles

vesicles now in synaptic cleft

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21
Q

ligand gated ion channels of chemical synapses of axon terminals

A

calcium: allows for neurotransmitter to release, the right amount enters to release the right amount of neurotransmitters- facilitated diffusion

neurotransmitter bind to ligand gated channel

change post synaptic cell permeability

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22
Q

fate of neurotransmitters of chemical synapses of axon terminals

A

enzymatically destroyed

reuptake into axon terminal by transport proteins

both are either or- if enzyme is available- will destroy- no reuptake

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23
Q

fate of neurotransmitters- enzymatically destroyed

A

enzyme in space

chemically/ enzymatically destroys neurotransmitter

faster

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24
Q

fate of neurotransmitters- reuptake into axon terminal by transport proteins

A

go back into presynaptic cell after job done (endocytosis)

get repackaged and used again

less manufacturing- less energy

reuptake: no enzyme to wipe out for neurotransmitter

slower

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25
Q

electrical synapses of axon terminals

A

ion current flows through gap juctions

smooth and cardiac muscle

26
Q

ion current flows through gap junctions of electrical synapses of axon terminals

A

cardiac: intercalated diks- gap junction

continuous cytoplasm

ions flow through- if enough get to threshold, create impulse

if enough flows through, can go to neighbor cell and cause it to contract

constant action due to gap junctions- peristalsis (patter of contraction)

27
Q

structure of skeletal muscles

A
  1. gross Anatomy and connective tissues
  2. Micro anatomy of skeletal muscle fibers
28
Q

gross Anatomy and connective tissues of skeletal muscle structure

A
  1. epimysium bundles together fascicles
  2. perimysium surrounds each fascicle
  3. endomysium surrounds each muscle cell (fiber)
  4. all are contiguous with tendons (or aponeuroses) and with periosteum
29
Q

epimysium bundles together fascicles

A

on surface

bundles all fascicles together

collection of cells

30
Q

perimysium surrounds each fascicle

A

saran wrap

surrounding fascicles

31
Q

endomysium surrounds each muscle cell (fiber)

A

innermost structures

deep inside muscle

cover every single cell

saran wrap around straws

32
Q

all are contiguous with tendons (or aponeuroses) and with periosteum

A

dense fibrous CT

muscular fascia

beyond edges of muscle

make tendon

33
Q

Micro anatomy of skeletal muscle fibers

A

smaller than cell
calcium helps shift the regulatory complex
1. Sarcolemma and sarcoplasm
2. multinucleate (myoblasts fuse to form myocytes)
3. myofibrils (actin and myosin)
4. Sarcomeres and striations
5. I-band, A-band, Z-lines, M-line, and H-zone
6. tropomyosin and troponin
7. sarcoplasmic reticulum (SR), transverse tubules (T tubes). and terminal cisternae

34
Q

Sarcolemma and sarcoplasm

A

sarcolemma- cell membrane of skeletal muscle cell

sarcoplasm- Cytoplasm of skeletal muscle cell

35
Q

nucleate (myoblasts fuse to form myocytes)

A

multiple cells fuse together

Can have hundreds

myoblasts create muscle

36
Q

myofibrils (actin and myosin)

A

Smaller than cell

inside cell

Made of actin and myosin- filaments

37
Q

Sarcomeres and striations

A

sarcomeres- between one Z line and another

Smallest section of muscle we can explain how contracts

striations

stripes

regular pattern of actin and myosin

Smooth muscle doesn’t have it

Use as landmarks

gone when muscle contract

When actin and myosin are both present the muscle looks darker which shows the striation

38
Q

I-band, A-band, Z-lines, M-line, and H-zone

A

i-band-only actin

z-line- zig zag

A-band- myosin and actin

h-zone- no overlap only myosin

m-line-no overlap

39
Q

tropomyosin and troponin

A

regulatory proteins

level of control when muscle contracts

stand in the way

blocking binding sites

to contract-binding sites have to be exposed

40
Q

sarcoplasmic reticulum (SR), transverse tubules (T tubes). and terminal cisternae

A

SR-specialized version endoplasmic reticulum

membranous

hollow

compartments

impulses for voltage gated ion channels

store stuff inside like calcium-uses active trasnport-let out by voltage gated ion channels

T-tubules- allow impulse to go down into cell

allow to spread throughout SR

like ground squirrel holes- go down hole and get to burrow

narrow until get to SR when spread out and get cell excited

uses to stimulate myofibrils in center of cell

terminal cisternae- holding tank for calcium

snuggles up to t-tubules

on ends

come spilling out of cisternae

triad: SR enlargement (terminal cisternae), t-tubule, SR enlargement (terminal cisternae)

voltage gated channels open- calcium diffuses with concentration gradient

continuous with cell membrane

41
Q

neuromuscular system

A
  1. motor units
  2. neuromuscular junction
  3. stimulus for contraction
42
Q

motor units

A

control: smallest-12-Gants motor (gross), largest-100s- fine motor

motor nerve and all cells it controls

every cell covered by endomysium except for place nerve communicates with muscle (neurotransmitter junction)

keeps cell receiving proper signal

43
Q

neuromuscular junction

A

post synaptic cell now muscle

motor neuron

axon terminal

open voltage gated calcium channels

vesicles fuse with membrane and spills contents

skeletal muscles neurotransmitter: acetylcholine

motor end plate

place with receptor for neurotransmitter

ligand gated

right underneath axon terminal

has to achieve threshold

enough acetylcholine bind to open voltage gated ion channels just outside motor end plate to send impulse along cell membrane

action potentials-all or nothing

synaptic cleft

acetylcholinesterase

enzyme that removes acetylcholine

44
Q

stimulus for contraction

A

release of acetylcholine (each, a type of neurotransmitter)

end plate potential and muscle action potential (muscle impulse)

calcium released from SR

45
Q

sliding filament model

A
  1. myofilaments do not shorten but slide over one another
  2. sarcomeres shorten, causing myofibrils to shorten
    3.areas of actin/myosin overlap increase
46
Q

myofilaments do not shorten but slide over one another

A

do not change length-orientation to each other changes

myofibrils do change length

z ines come closer together

each sarcomere becomes shorter

47
Q

sarcomeres shorten, causing myofibrils to shorten

A

myosin bent

pulls actin toward center little bit over and over

myosin heads like someone doing freestyle- don’t attach at once- some pulling forward- other repositioning

otherwise if all detach/ attach at once it would go back to start

48
Q

areas of actin/myosin overlap increase

A

myosin and actin haven’t changed length

h zone, I band and z lines shorten, smaller, some almost gone

multiply to all sarcomeres

49
Q

excitation-contraction

A

excitatory post synaptic potential has to happen for muscle to contract

excitatory response leads to contraction- has to happen- go together

Motor neuron releases acetylcholine

ligand gated channels on sarcolemma open

Na+ and K+ channels open (Na+ influx predominates)

end plate potential results, threshold achieved, voltage gated Na+ channels open

sarcolemma and t tubules depolarize

voltage gated channels on sarcoplasmic reticulum open

calcium released into sarcoplasm by diffusion

calcium binds to troponin, shifts regulatory proteins

actin and myosin change position relative to one another

50
Q

cross bridge cycling

A

ATP and cross bridge formation

ATP binds to myosin, hydrolyzes (ATP→ ADP + P)

activated myosin binds to actin

ADP released, myosin head pivots (power stroke)

New ATP binds, myosin detaches from actin

hydrolysis of new ATP returns myosin to activated position

cross bridge cycling continues as long as Ca2+ and ATP available

relaxation

rigor mortis

51
Q

ligand gated channels on sarcolemma open during excitation-contraction

A

Na+ enter

52
Q

end plate potential results, threshold achieved, voltage gated Na+ channels open during excitation-contraction

A

run impulse or series of action potentials

53
Q

voltage gated channels on sarcoplasmic reticulum open of excitation-contraction

A

cisternae of SR store calcium

Ca+ in SR due to active transport

t tubule and surrounding cisternae= triad membranes

54
Q

actin and myosin change position relative to one another of excitation-contraction

A

I band, H zone become shorter

z lines pulled toward m line

55
Q

ATP and cross bridge formation during cross bridge cycling

A

relaxed muscle

heads not attached

binding sites not visible

ATP interacts with myosin and is split into ADP and P

ATP is committed to myosin molecules

myosin heads activated and energized even though binding sites arent exposed

56
Q

activated myosin binds to actin during cross bridge cycling

A

Ca+ released from SR due to nerve signal

regulatory proteins shifted

binding sites exposed

myosin heads attached to binding sites of actin

head in cooked position

like bow being pulled back- needs energy

57
Q

ADP released, myosin head pivots (power stroke) during cross bridge cycling

A

myosin power stroke forward

actin sliding across surface

myosin stays put

ADP and P released

bow being released- don’t need energy

58
Q

New ATP binds, myosin detaches from actin during cross bridge cycling

A

new ATP binds-for every myosin head- needs separate ATP molecule

start over

detach myosin heads into coked position

not all will detach at once

otherwise muscle will just go back to beginning

freestyle instead of buttefly

59
Q

hydrolysis of new ATP returns myosin to activated position during cross bridge cycling

A

ATP splits

energy contained is committed

myosin heads cocked in ready position

60
Q

cross bridge cycling continues as long as Ca2+ and ATP available during cross bridge cycling

A

if binding sites are open (due to Ca+ and stimulus)

61
Q

relaxation of cross bridge cycling

A

requires energy

Ca+ removed

ATP is needed for active transport of Ca+ into SR (storage)

causes tropomyosin to shift

binding sites no longer exposed

VG Ca+ channels need to close

impulse needs to stop and contraction stops

have to start at beginning

with motor neuron, then NT, …

62
Q

rigor mortis of cross bridge cycling

A

state of muscle stiffness due to death

no new ATP is made- continuous muscle contraction

Ca+ still available- diffuse out of SR to shift regulatory proteins- no ATP to bring back to SR

ATP was already committed to action

power stroke will occur

no ATP to break actin and myosin bond

contraction of muscle will be continuous with no relaxation

will dissipate through time

A&P (5 decks)

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