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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
electrical synapses of axon terminals
ion current flows through gap juctions smooth and cardiac muscle
26
ion current flows through gap junctions of electrical synapses of axon terminals
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
structure of skeletal muscles
1. gross Anatomy and connective tissues 2. Micro anatomy of skeletal muscle fibers
28
gross Anatomy and connective tissues of skeletal muscle structure
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
epimysium bundles together fascicles
on surface bundles all fascicles together collection of cells
30
perimysium surrounds each fascicle
saran wrap surrounding fascicles
31
endomysium surrounds each muscle cell (fiber)
innermost structures deep inside muscle cover every single cell saran wrap around straws
32
all are contiguous with tendons (or aponeuroses) and with periosteum
dense fibrous CT muscular fascia beyond edges of muscle make tendon
33
Micro anatomy of skeletal muscle fibers
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
Sarcolemma and sarcoplasm
sarcolemma- cell membrane of skeletal muscle cell sarcoplasm- Cytoplasm of skeletal muscle cell
35
nucleate (myoblasts fuse to form myocytes)
multiple cells fuse together Can have hundreds myoblasts create muscle
36
myofibrils (actin and myosin)
Smaller than cell inside cell Made of actin and myosin- filaments
37
Sarcomeres and striations
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
I-band, A-band, Z-lines, M-line, and H-zone
i-band-only actin z-line- zig zag A-band- myosin and actin h-zone- no overlap only myosin m-line-no overlap
39
tropomyosin and troponin
regulatory proteins level of control when muscle contracts stand in the way blocking binding sites to contract-binding sites have to be exposed
40
sarcoplasmic reticulum (SR), transverse tubules (T tubes). and terminal cisternae
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
neuromuscular system
1. motor units 2. neuromuscular junction 3. stimulus for contraction
42
motor units
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
neuromuscular junction
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
stimulus for contraction
release of acetylcholine (each, a type of neurotransmitter) end plate potential and muscle action potential (muscle impulse) calcium released from SR
45
sliding filament model
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
myofilaments do not shorten but slide over one another
do not change length-orientation to each other changes myofibrils do change length z ines come closer together each sarcomere becomes shorter
47
sarcomeres shorten, causing myofibrils to shorten
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
areas of actin/myosin overlap increase
myosin and actin haven’t changed length h zone, I band and z lines shorten, smaller, some almost gone multiply to all sarcomeres
49
excitation-contraction
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
cross bridge cycling
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
ligand gated channels on sarcolemma open during excitation-contraction
Na+ enter
52
end plate potential results, threshold achieved, voltage gated Na+ channels open during excitation-contraction
run impulse or series of action potentials
53
voltage gated channels on sarcoplasmic reticulum open of excitation-contraction
cisternae of SR store calcium Ca+ in SR due to active transport t tubule and surrounding cisternae= triad membranes
54
actin and myosin change position relative to one another of excitation-contraction
I band, H zone become shorter z lines pulled toward m line
55
ATP and cross bridge formation during cross bridge cycling
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
activated myosin binds to actin during cross bridge cycling
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
ADP released, myosin head pivots (power stroke) during cross bridge cycling
myosin power stroke forward actin sliding across surface myosin stays put ADP and P released bow being released- don’t need energy
58
New ATP binds, myosin detaches from actin during cross bridge cycling
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
hydrolysis of new ATP returns myosin to activated position during cross bridge cycling
ATP splits energy contained is committed myosin heads cocked in ready position
60
cross bridge cycling continues as long as Ca2+ and ATP available during cross bridge cycling
if binding sites are open (due to Ca+ and stimulus)
61
relaxation of cross bridge cycling
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
rigor mortis of cross bridge cycling
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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