week 3: 10.4 Flashcards
typical resting membrane potential in unstimulated neurons and skeletal muscle fibers
-70mV
-85mV
what is the membrane potential
measure of cellular polarisation that compares the cytoplasmic membrane surface charge to the extracellular surface charge
depolarisation
influx of sodium ions leads to depolarisation as membrane potential becomes less negative
hyperpolarisation
movement of potassium ions out of a cell leads to hyperpolarisation as membrane potential becomes more negative
repolarisation
return to resting potential
what do neurons and skeletal muscle fibres have
electrically excitable membranes
what do excitable membranes permit
rapid communication between different parts of a cell
what does depolarisation and repolarisation cause in neurons and skeletal muscle fibers
action potential (electrical impulse)
that is propigated along their plasma membranes
what do excitable membranes contain
voltage-gated ion channels
what are voltage gated ion channels activated and inactivated by
changes in membrane potential
when do the electrical channels become activated
when the membranes of neurons and skeletal muscle fibers first depolarise from resting potential to threshold potential
threshold potential of neurons
-60mV
threshold potential of skeletal muscle fibers
-55mV
upon reaching threshold potential,
voltage-gated sodium ion channels open and there is a rapid influx of positively charged sodium ions into a cell
what causes the closure of the voltage gated sodium ion channels
depolarisation peaks at a membrane potential of +30mV
how does repolarisation of membrane begin
voltage-gated potassium ion channels open and positively charged potassium ion leave the cell
what causes the membrane potential to become negative again
the loss of the more positive charges than entered the cell
what happens during refractory period
former conc of sodium and potassium ions across cell are restored through sodium-potassium ion pumps
why does action potential travel in one direction
Further depolarisation cannot occur until the refractory period is over
prevents action potential propagating back from where it came from
skeletal muscles fibers cannot begin contracting until,
they recieve instructions from motor neurons of the CNS
how do motor neurons carry instructions
in the form of action potentials
when does a contraction of a skeletal muscle fiber begin
sarcoplasmic reticulum releases stored calcium ions into the cytosol of the muscle fiber
when does a skeletal muscle fiber contraction end
as the intracellular calcium ions are reabsorbed
neuromuscular junction
synapse of a skeletal muscle fiber and a neuron
what is the NMJ made up of
axon terminal
motor end plate
synaptic cleft (in between)
what is the motor end plate
specialised region of the sacrolemma
what is a neurotransmitter
a chemical released by a neuron to change the permeability or other properties if another cell’s plasma membrane
what does the cytoplasm of the axon terminal contain
vesicles filled with molecules of ACh
what does the synaptic cleft and motor end plate contain
molecules of the enzyme AChE which breaks down ACh
what is the synaptic cleft
narrow space that separates the axon terminal of the neuron from the opposing motor end plate
what is the stimulus for ACh release
arrival of action potential at the axon terminal
what happens when AP reaches neurons axon terminal
permeability changes in its membrane, triggers the exocytosis of ACh into synaptic cleft
exocytosis occurs as,
vesicles fuse with the neruron’s plasma membrane
once ACh is released into synaptic cleft,
diffuse across synaptic cleft
bind to ACh receptor membrane channels
what does ACh binding to ACh receptor channels cause
opens the membrane channel on the surface of the motor end plate
sodium ions movement and why
sodium ions rush into the cytosol
becuase extracellular fluid contains high conc of sodium ions and sodium ion conc inside cell is vey low
what results in the generation of the action potential in the sarcolemma
sudden inrush of sodium ions
how is ACh removed from the synaptic cleft
diffuses away from synapse
or
broken down by AChE
what is ACh broken down into by AChE
acetic acid and choline
why is the removal of ACh important
leads to the closing of ACh receptor membrane channels
excitation contraction coupling
link between the generation of action potnetial in sacrolemma and the start of a muscle contraction
where does the excitation contraction coupling occur
at the triads
what happens when action potential reaches a triad
triggers the release of Ca2+ from the terminal cisternae of the sarcoplasmic reticulum
how long does the change in permeability of the SR to Ca2+ last
0.03 seconds
[Ca2+] in and around sarcomere after AP reaches triad
100 times resting level
why is the effect of calcium ion release almost instantaneous
because terminal cisternae are loacted at zones of overlpa where thick and thin filaments ineract
calcium ions binding to troponin
changes the shape of the troponin molecule
weakens the bond between troponin and actin
troponin molecule changes position rolling the attached tropomyosin strand away from the active sites
contraction cycle begins
contraction cycle
series of molecular events that enable muscle contraction
after active sights are exposed
myosin heads bind to them forming cross bridges
connection between head and tail
functions as a hinge that leads the head pivot
pivots using energy released from hydrolysis of ATP
head swings towards the M line-power stroke
pivoting is the key step in muscle contraction
what is the power stroke
when the head swings towards the M line
what happens when muscle cells contract
they pull on the attached tendon fibers
what type of force is tension
active- energy must be expended to produce it
what must applied tension overcome before movement can occur
the objects load (or resistance)
what is an objects load/ resistance
a passive force that opposes movement
what does the load of an object depend on
weight, shape, friction ect
when does the object move
when applied tension exceeds the load
what is compression (force)
push applied to the object, tends to force object away from source of compression
no movement can occur until applied compression,
exceeds load of object
why can muscle cells pull but not push
muscle cells can use energy to shorten and generate tension through interaction between thick and thin filaments, but not to lengthen and generate compression
what does each power stroke result in
sarcomere shortened by 0.5 %
why does the entire muscle shorten at the same rate
all the sarcomeres contract together
what does the speed of the sarcomere shortening depend on
the cycling rate- the number of power stroeks per second
relationship between load and cycling rate
the greater the load, the slower the cycling rate
duration of contraction depends on
- period of stimulation at NMJ
- presence of free calcium ions in cytosol
- availability of ATP
contraction will continue if
additional action potentials arrive at NMJ in rapid sucession
what does a series of action potentials arriving at the NMJ causing the continual release of ACh produce
series of action potentials in the sarcolemma that keeps Ca2+ levels elevated in cytosol
