chap 9 muscular system II Flashcards
how do the nerves from the brain and spinal cord extend to the skeletal muscle
through the axons
what do axons do?
convey electrical signals to muscle cells and initiate contraction
what is RMP?
resting membrane potential
like a charged battery ready to do work
what is the voltage inside the cell
-70 mV
what creates and maintains an imbalance of Na+ and K+?
active transport of Na+/K+ by membrane pump
what do CLOSED ion specific gates do?
prevent Na+/K+ from seeking rapid equal concentration adjustments by diffusion
other ion specific gates
ligand activated gates
voltage activated ion gates
how do ligand activated gates work?
are activated by a ligand landing on the receptor protein of the gate
how is ligand released?
due to some signal
how do voltage activated ion gates work?
opened by a rapid change in voltage within the cell
example of a voltage activated ion gate?>
potassium gate
what is depolarization?
reversal of the voltage difference
inside grows less negative
how does depolarization work
a stimulus to the cell causes some Na+ ion specific gates to open, causing Na+ to leak into the cell
this creates a voltage change
electrical charge for outside Na+
outside + positive
electrical charge for inside K+
inside - negative
what happens when threshold is reached?
if the stimulus is strong enough to cause sufficient voltage change, Na+ specific voltage gates quickly open completing rapid intense depolarizatikn
what happens to the electrical charge during depolarization?
goes from -70mV to +30mV as Na+ move in
what happens if threshold is not reached?
no action potential takes place
what is action potential?
the rapid changing of membrane potential
what is the all or none principle
if the ligand-gated Na+ entry is above threshold, then no more neurotransmitter ligand is necessary to open the rest of the voltage gated channels and complete the action potential
repolarization
put membrane back to RMP
steps of repolarization
with the abundance of Na+, charge is +30. this trigggers the K+ specific voltage gated channels to open
K+ then rushes out, using laws of diffusion
intracellular environment returns to -70mV, returning to RMP
homeostasis
an ion imbalance across the membrane must exist or ions will not move or move as rapidly when gates are opened
what help maintain the -70mV during RMP
Na+/K+ pump
propagation
spreading of a signal throughout the cell
result of propagation
muscle cells contract, nerve cells send impulses
what happens if they is repeat stimulation?
action potentials increase the strength of the cell response which results in an increase in strength or duration of contraction in muscle cells
synapse
neuromuscular junction
transfer site of motor neuron action potential to skeletal muscle cell action potential
what stimulates each muscle fiber
the terminal branch of axon
structures of neuromuscular junction
presynaptic terminal
synaptic cleft
postsynaptic membrane
presynaptic terminal
the end
sends the message
postsynaptic membrane
“motor end plate”
skeletal muscle cells
steps of neuromuscular junction
- action potential travels down moto neuron membrane to the presynaptic terminal
- Ca2 specific voltage gates open and Ca2+ diffuses inwards
- triggers neurotransmitter vesicle release by exocytosis into the synapse
- result of action potential across the muscle fiber
acetylcholine
ACh
is the excitatory NT of the NMJ
what happens after the exocytosis into the synapse
ACh ligand binds to ACh receptors on muscle fiber post synaptic membrane activating ligand gate Na+ channels
depolarization of the postsynaptic membrane generates action potential
what happens to ACh?
ACh is quickly broken down
ACh-> acetic acid + choline
purpose of choline
to be reuptaked to more more ACh
acetic acid
bad
formed from a variety of metabolic responses
enzyme responsible for ACh breakdown
acetylcholineesterase AChE
result of action potential across the muscle fiber
excitation-contraction coupling
steps after action potential created
excitation-contraction coupling
1) T-tubule invagination takes the sarcolemma depolarization into the S
2) Ca2+ is released internally (200x normal concentration_
3) Ca2+ binds to the regulatory troponin and exposes myosin binding site
4) myosin head engages and power stroke ensues
5) ATP molecule energy uses to unhook myosin and recock head
what do organophosphate pesticides and some nerve gases do?
block the action of AChE
result in transient spastic paralysis
spastic transient paralysis
fibers constantly stimulated, unable to relax and eventually fatigue
death through respiratory failure
importance of protecting populations and workers from sprays
why would solders be given syringes of atropine sulfate which blocks postynaptic membrane ACh receptor sites?
??
what happens to blocked postynaptic membrane ACh receptors
limits membrane depolarization
flaccid paralysis results
myasthenia gravis
flaccid paralysis
muscles unable to respond
myasthenia gravis
your antibodies from response to viral infection damage ACh receptors
muscle weakness
most survive but end up in coma and require ventilation
treatment for myasthenia gravis
neostigmine, which interferes with AChE action, tries to keep whatever ACh is already there
recovery stroke
ATP dependent release of myosin head and recocking
what is muscle contraction?
produced by many quick repeats of the cycle in each fiber that has been stimulated by the neuron
what happens when no more stimulus is present?
relaxation of muscle tissue
Ca2+ are rapidly moved back into the SR by active transport (ATP needed)
rigor mortis
stiffness that covers body several hours after death. loss of intracellular containment of the Ca2+ and lack of ATP causes constant increasing contractions (rigor) in the hours after death.
after 24 hours the muscle cell proteins will deteriorate and begin to relax
