U5 Lecture 40 Flashcards
where does an action potential travel along
the axon of motor neuron to the presynaptic terminal on the muscle fiber
what does depolarization of terminal open and trigger
it opens calcium channels to trigger release of acetylcholine (Ach)
where does acetylcholine bind
to nicotinic Ach receptors on muscle
what is excess acetylcholine destroyed by
acetylcholinesterase
binding of Ach to receptors opens what
ligand gated sodium channel to cause large muscle depolarization which triggers muscle action potential in healthy individual
action potential triggers calcium release from where which allows what?
release from sarcoplasmic reticulum which allows sliding of actin/myosin filaments due to cross bridges
where does calcium return to after cross bridge formation
the sarcoplasmic reticulum
what happens in motor neuron degeneration or conduction failure
efferent action potentials fail to reach effector, either due to motor neuron degeneration or loss of myelin on axons
what is an example of motor neuron degeneration
amyotrophic lateral sclerosis
what is an example of conduction failure
multiple sclerosis
what happens in neuromuscular transmission failure
motor neuron action potential arrives at neuromuscular junction but fails to cause sufficient muscle excitation
what is an example of neuromuscular transmission failure
lambert eaton syndrome or myasthenia gravis
what happens in dystrophic myopathies
weakness and loss of muscle fibers
what is an example of dystrophic myopathies
muscular dystrophy
what happens in metabolic myopathies
a variety of inherited metabolic disorders in which genes encoding enzymes that aid glucose metabolism or ATP production in muscle are mutated
what is an example of metabolic myopathies
mcardles myopathy
what is problem #1 preliminary diagnosis
- patient presents with weakness
- difficulty standing up from seated position or lifting objects
- decreased street reflex
- minor atrophy of muscle tissue
what are the take home messages for problem #1
- motor neuron action potential normally leads to muscle fiber action potential because so much Ach is released and there are plenty of Ach receptors “high safety factor”
- failure of neuromuscular transmission can prevent the activation of muscle contraction causing weakness. the resultant extended dishes can lead to muscle atrophy. note that this is the opposite of the training effects discussed in the first integration lecture
what is the question of problem #2?
what is the specific problem with patient’s neuromuscular synaptic transmission?
what is lambert eaton syndrome
- autoimmune disorder in which the body produces antibodies against voltage gated calcium channels in its own presynaptic terminals
- this results in decreased release of Ach from presynaptic terminals, failure to cause an actin potential in the muscle fiber and therefore muscle weakness
what is myasthenia gravis
- autoimmune disorder in which body produces antibodies against nicotinic ACh receptors at its own neuromuscular junction
- this results in failure of ACh to open enough ligand-gated channels in postsynaptic membrane, failure of muscle action potential and therefore muscle weakness
acetylcholinerase inhibitors are drugs such as
neostigmine, physostigmine or endrophonium
how can Ach be applied directly to a muscle fiber
using a small pipette to spritz some out
what are the take home messages for problem #2
- autoimmune disorders can disrupt neuromuscular transmission by attacking presynaptic calcium channels or postsynaptic Ach receptors
- using our knowledge of the steps required for normal synaptic transmission, we can devise a way to differentiate between lambert eaton and myasthenia gravis
