Lecture 9.2 main points Flashcards
what must happen in order for electrical signals in motor neurons to be communicated to muscle
electrical signals (action potentials) from motor neurons must be transformed into chemical signals ( neurotransmitters)
where does the electrical signal in motor neurons communication to muscle
at the neuromuscular junction
as a result of the electrical signals, what do the chemicals cause in a muscle cell
chemical signals then stimulate electrical signals in sarcolemma of the muscle fiber ( if strong enough)
the electrical signal in the muscle fiber (action potential) then activate a series of events that leads to the shortening of the skeletal muscle fiber
what is the predominant theory of skeletal muscle contraction
sliding filament model of contraction
brief description of sliding filament model of contraction
interactions between thick and thin filaments of the sarcomere produce the contraction (shortening) of a skeletal muscle cell
-in a relaxed state, thin and thick filaments overlap slight
-during contraction thin filaments slide toward the M-line past the thick filaments (acting and myosin overlap more)
chemical gradients of certain ions are necessary for what
proper electrical, and contractile activity of skeletal muscle
three main ions in muscle cells. concentration at rest intracellular vs extracellular
intracellular [Ca] very low
intracellular [Na] very low
intracellular [K] high
what is the numeric value of intracellular charge at rest
-95 mV
what is the extracellular charge at rest
0 mV
what two events must occur for skeletal muscle to contract
activation and excitation-contraction coupling
how does activation occur and what must it generate
must be nervous system stimulation, must generate action potential in sarcolemma
happens at the neuromuscular junction
what does action potential (excitation) produce that is necessary for contraction
action potential propagated along sarcolemma
intracellular Ca levels must briefly rise leading to the onset of contraction
list the steps in sequence for phase 1 in which the motor neuron stimulates the muscle fiber (activation)
AP arrives at axon terminal at neuromuscular junction
Ach is released, binds to receptors on sarcolemma
Ion permeability of sarcolemma changes
Local change in membrane (depolarization) occurs
Local depolarization (end plate potential) ignites the AP in sarcolemma
list the steps in sequence for phase 2 in which excitation (action potential) - contraction coupling occurs
AP travels across the entire sarcolemma
AP travels along T tubules
SR releases Ca, Ca binds to troponin,
myosin binding sites on actin exposed
myosin heads bind to actin, contraction begins
what type of neuron connects to, and stimulates, a skeletal muscle cell, is it voluntary or involuntary
somatic motor neurons, voluntary
how do somatic motor neuron axons travel to skeletal muscle
travel via nerves (bundles of mostly neuron axons)
are somatic motor neuron axons branched or unbranched
may form several branches as it enters the whole muscle
each axon ending forms a neuromuscular junction with what
a single muscle fiber
events of the motor neuron at the NMJ (neuromuscular junction)
- action potential arrives at the axon terminal of motor neuron
- voltage gated Ca channels open. Ca enters the axon terminal moving it down its electrochemical gradient
- Ca entry causes Ach to be released by exocytosis
- Ach diffuses across the synaptic cleft and binds to its receptors on the sarcolemma
- Ach binding opens ion channels in the receptors that allow SIMULTANEOUS passage of Na INTO the muscle fiber and K OUT OF the muscle fiber
more Na enters than K exits which produces a local charge in the membrane potential called the end plate potential - Ach effects are terminated by its breakdown in the synaptic cleft by acetylcholinerase and diffusion away from the junction
at the NMJ do calcium channels open or close briefly
open briefly allowing calcium to enter the axon terminal
at the NMJ what ion moves through the channel and where does it go
calcium moves through the channel and goes into the cell
what is the purpose of calcium inside the axon terminal? What does it cause?
causes acetylcholine to be release by exocytosis
what is the neurotransmitter used for chemical communication between the motor neuron and skeletal muscle fiber
Ach (acetylcholine)
into what space is acetylcholine released
the synaptic cleft
what Ach destroying enzyme waits in the synaptic cleft
acetylcholinesterase
why is acetylcholinesterase important
breaks down Ach to acetate and choline
prevents continued muscle fiber contraction in the absence of addition stimulation
as Ach makes it to the surface of the muscle cell at the NMJ what receptor does it bind to?
nicotinic acetylcholine receptor (nAchr)
as Ach binds to nAchr does the ion channel open or close
open
what two ions are allowed to pass through the post synaptic ion channel
sodium and potassium
sodium in, potassium out
does Na or K flow through the channel in greater amounts in the post synaptic membrane
Na
what effect does the ion flow have on the membrane charge of -95mV
makes it more positive, depolarization
the change in sarcolemma membrane charge at the NMJ is called what
end plate potential
is the end plate potential a local event or entire cell event
local, only happens at the NMJ not on the whole cell
what is depolarization
when the membrane voltage gets closer to zero from its initial -95. Becomes less polar (different)
what chemical directly affects the release of acetycholine
calcium
term for critical value voltage that must be reached in order to illicit an action potential
threshold
once threshold is reached, what ion channels open in large amounts
voltage gated sodium channels
what do voltage gated sodium channels allow to pass
sodium into the cell
what is the effect on the intracellular membrane voltage with the increasing flow of sodium into the cell
intracellular membrane voltage becomes more positive
what phase of AP generation involves the opening of sodium channels called
depolarization phase
what phase follows depolarization and what does it do for the electrical condition of the membrane voltage (intracellular)
repolarization, becomes less negative due to more potassium exiting than sodium entering
during repolarization many voltage gated sodium channels begin to close, what channels begin to open
voltage gated K channels
during repolarization, as sodium channels close, what happens to the amount of sodium flowing into the cell
decreases the influx of sodium
during repolarization as potassium channels begin to open what happens to potassium flow outside of the cell
potassium flow more rapidly outside of the cell
what is the effect of lessening sodium influx into the cell and increasing potassium efflux out of the cell, does the intracellular membrane voltage change?
intracellular membrane voltage becomes more negative
what happens when potassium channels close
membrane potential is restored back to resting
what cannot happen during the refractory period
another action potential cannot be stimulated
what is the latent period
when E-C (excitation- contraction) coupling events occur, time between AP initiation and beginning of contraction
certain voltage-sensitive proteins are found in the membrane of the T-Tubule, what is their name
DHP receptors
what ion passes through DHP receptors
small amounts of calcium to flow into the sarcoplasm
DHP receptors are connected to special protein channels called what
Ryanodine receptors
where are ryanodine receptors found
in the terminal cisterns of the sarcoplasmic reticulum
what is the function of ryanodine receptors
to release calcium from the sarcoplasmic reticulum into the sarcoplasm
when stimulated by DHP receptors, ryanodine receptors allow what ion to pass through their channel
calcium
where does the calcium flow when passed through ryanodine receptors
from the sarcoplasmic reticulum into the sarcoplasm
how does the influx of calcium ions into the sarcoplasm affect sarcoplasmic Ca concentration
it increases
excitation coupling events
single muscle AP causes brief activation of DHP receptors followed by activation of the ryanodine receptords allowing a brief release of calcium into the sarcoplasm. the DHP receptors deactivate therefore closing the Ryanodine receptors, ending the release of Ca into the sarcoplasm
what happens if after the first AP there isn’t a subsequent
sarcoplasmic Ca will fall due to removal by SERCA pumps - pumping calcium back into the SR and sarcolemma ATPases that pump calcium out of the cell
