exam 3 Flashcards
action potential
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
Suprathreshold and the all or none principle of action potential
Doesn’t matter if you barely got to the threshold, you got there
all responses are alike
All leak channels stay open, Na+/K+ pump continues working of action potential
not permeable to sodium
at stimulus noting changes on axon until it gets to threshold
threshold reached of action potential
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
depolarization phase, voltage gated Na+ channels of trigger zone open of action potential
Big upswing
peak phase of action potential
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
why do channels inactivate
Each action potential is individualized
has to go from the beginning to the end before starting again
Can’t have summation
relative refractory period
Respond if have two
Relatively larger stimulus to be able to respond
Not at a normal resting potential
repolarization phase of action potential
reduced influx Na+
Potassium exiting by moving with the gradient
The inside goes back to negative
voltage gated K+ channels remain open
Hyperpolarization phase Of action potential
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
After hyperpolarization phase
voltage gated K+ channels close
membrane potential returns to resting value
look at picture for excitable cells
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action potential propogation
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`
positive feedback - action potential propagation
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
influence of axon diameter- action potential propogation
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
influence of myelin - action potential propogation
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
Axon terminals
chemical synapses- always have space, requires energy: make neurotransmitter, release the proteins
electrical synapses
chemical synapses of axon terminals
voltage-gated calcium channels
vesicles maintaining neurotransmitter
exocytosis
ligand gated ion channels
fate of neurotransmitters
vesicles maintaining neurotransmitter of chemical synapses of axon terminals
spherical sac
contains protein (neurotransmitter)
exocytosis of chemical synapses of axon terminals
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
ligand gated ion channels of chemical synapses of axon terminals
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
fate of neurotransmitters of chemical synapses of axon terminals
enzymatically destroyed
reuptake into axon terminal by transport proteins
both are either or- if enzyme is available- will destroy- no reuptake
fate of neurotransmitters- enzymatically destroyed
enzyme in space
chemically/ enzymatically destroys neurotransmitter
faster
fate of neurotransmitters- reuptake into axon terminal by transport proteins
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
electrical synapses of axon terminals
ion current flows through gap juctions
smooth and cardiac muscle
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)
structure of skeletal muscles
- gross Anatomy and connective tissues
- Micro anatomy of skeletal muscle fibers
gross Anatomy and connective tissues of skeletal muscle structure
- epimysium bundles together fascicles
- perimysium surrounds each fascicle
- endomysium surrounds each muscle cell (fiber)
- all are contiguous with tendons (or aponeuroses) and with periosteum
epimysium bundles together fascicles
on surface
bundles all fascicles together
collection of cells
perimysium surrounds each fascicle
saran wrap
surrounding fascicles
endomysium surrounds each muscle cell (fiber)
innermost structures
deep inside muscle
cover every single cell
saran wrap around straws
all are contiguous with tendons (or aponeuroses) and with periosteum
dense fibrous CT
muscular fascia
beyond edges of muscle
make tendon
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
Sarcolemma and sarcoplasm
sarcolemma- cell membrane of skeletal muscle cell
sarcoplasm- Cytoplasm of skeletal muscle cell
nucleate (myoblasts fuse to form myocytes)
multiple cells fuse together
Can have hundreds
myoblasts create muscle
myofibrils (actin and myosin)
Smaller than cell
inside cell
Made of actin and myosin- filaments
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
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
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
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
neuromuscular system
- motor units
- neuromuscular junction
- stimulus for contraction
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
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
stimulus for contraction
release of acetylcholine (each, a type of neurotransmitter)
end plate potential and muscle action potential (muscle impulse)
calcium released from SR
sliding filament model
- myofilaments do not shorten but slide over one another
- sarcomeres shorten, causing myofibrils to shorten
3.areas of actin/myosin overlap increase
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
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
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
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
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
ligand gated channels on sarcolemma open during excitation-contraction
Na+ enter
end plate potential results, threshold achieved, voltage gated Na+ channels open during excitation-contraction
run impulse or series of action potentials
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
actin and myosin change position relative to one another of excitation-contraction
I band, H zone become shorter
z lines pulled toward m line
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
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
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
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
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
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)
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, …
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
