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26 Cards in this Set
- Front
- Back
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What is the presynaptic neuron called and where does it usually receive its activation for voluntary motion?
What is released after activated and what does that cause? |
a-motor neuron
activated from cortex - Releases glutamate or aspartate - causes EPSP- sodium influx |
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How does the axon of the a-motor neuron leave the spinal cord?
Describe three characteristics... |
1. via the ventral root
a. large diameter b. heavily myelinated for fast conduction velocity c. has a short refractory period |
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Describe the structure of Neuromuscular junction..
and presynaptic terminal.. |
a. Axons originate in brain or spinal cord
b. Axons branch as the approach muscle fibers (branching called arborization) Pre- lots of mitchondria, clear vesicles with Ach inside, choline- I acetyltransferase |
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Describe some of the features of the a-motor neuron...
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a. axons are divided into fine branches that lie in shallow depression at surface of muscle fiber
b. postsynaptic area- is oval motor end plane is hidden underneath the neural component |
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What is green and red?
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Green- axons
Red- Ach |
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What would happen if the a-motorrneuron were not present on a muscle?
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W/o it muscle would die unless it found additional innervation
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After Ach binds to Ach nicotinic receptor in motor neuron and what happens next?
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Na channel under goes confirmational change and Na goes into the cell causing an influx.
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Is end-plate potential (epp) a local event or true action potential?
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Local and graded depolarization. Not an action potential because no Na voltage gate channels.
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After vesicular docking with calcium what proteins are involved in pulling the vesicle to the membrane and allowing fusion to the membrane...
What does botulism and tetanus toxins do to muscles and proteins involved in this? |
synaptobrevin (VAMP) and SNAP
the toxin from botulinum hydrolyzes VAMP and causes flaccid paralysis Tetanus acts on VAMP, not at NMJ in spinal cord leads to spasticity |
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Describe what effect activation of the receptors on the motor endplate has in the skeletal muscle.
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- causes end plate potential... binding to channel causes sodium channels to open which causes slight depolarization...
- eventual contraction of muscle and action potentials in post synaptic cell only after sodium from channels cause cell's voltage gated channels to open |
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Describe nAchR...
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nicotinic acetylcholine recepters have 5 subunits
a. 2 alpha subunits b. each alpha contains Ach binding site |
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Describe the numerical ratio of action potentials in the motoneuron to action potentials in the muscle.
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1:1 every motoneuron action potential IS SUPPOSED TO lead to one in the skeletal muscle cell
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Describe how skeletal muscle contraction can be inhibited and role of enzyme...
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1. Ach's chemical signal must be destroyed!
2. Acetylcholinesterase- enzyme that is in synaptic cleft, bound to post synaptic and presynaptic membrane - breakes Ach into acetate (diffuses out) and choline- reuptake to presynaptical terminal and made into Ach |
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Compare and contrast the miniature end-plate potential, the end-plate potential, and the action potential.
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mEPP- smaller spontaneous depolarization of the motor end plate due to Ach released from a-motoneuron that spontaneously fuses with pre-synaptic a-motoneuron membrain
EPP- results in action potential and mEPP does not |
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Explain rapsyn's relationship with nAchR in maintaining the health of the neuromuscular junction...
What happens when denervation (loss of a-motoneuron) occurs? |
Rapsyn is a protein that binds and anchors nAchR in place at the junctional folds
Denervation- nAchR and rapsyn dissociate and nAchR wander around skeletal muscle's membrane and... i. can be activated from Ach from diffused Ach or Ach in blood ii. leads to isolated muscle twitches (fasciculations) |
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Why would cutting a motoneuron from muscle cause muscle cell to eventually die?
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Due to lose of other "trophic" factors usually released by nerve no longer released...
a. Agrin released into synaptic cleft and binds to receptor associated with MuSK (muscle specific kinase). b. binding promotes rapsyn/AchR aggregation and muscle cell will survive |
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What is denervation hypersensitivity?
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a-motoneuron damage/destruction resulting in spontaneous contractions of isolated regions of the skeletal muscle
Rapsyn does not associate with nAchR and nAchR wanders and randomly binds making isolated contractions |
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How does cholinesterases such as carbochol, methacholine, and nicotine in high doses cause muscle paralysis?
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They remain on binding sites of receptors thus Na+ keeps coming in which makes the voltage gated Na channels which opened after depolarization locked in inactive state... therefore since voltage gated channels can not re-open muscles can not contract (i.e. paralized like a mug!)
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What type of drugs prevent action of Ach binding to nAchR?
Give a specific example one... |
Curariform drugs
a. D-tubocurarine- competitive antagonist- binds to Ach site w/o opening Na gate |
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What drugs inhibit Acetylcholinesterase?
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1. stigmines
2. organophosphates |
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What is cause of myasthenia gravis and what are treatments?
What are physical symptoms? |
a. autoimmune Abs respond to Ach receptors but body continues to make new receptors so Acetylcholinesterase inhibitors are used to keep Ach around
b. generalized weakness |
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What is cause of ALS?
What is clinical presentation? How is it treated? |
a. death of motor neurons due to oxidative stress after mutation of Superoxide Dismutase (SOD)--- causes Degeneration hypersensitivity, losing agrin, twitches due to random Ach binding, eventual muscle death (atrophy) due to lose of trophic properties (i.e. agrin/MuSK--> rapsyn/AchR)
b. spasms in muscles most evident in extremities- odd quality in voice, atrophied muscle c. No good treatments yet |
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Why would a mutation in SOD (superoxide dismutase) which causes more oxidative stress on a neuron affect the motor neurons more than other ones?
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motoneurons use a large quantity of oxygen so are affected more
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What diseases result from the following...
a. Superoxide Dismutase b. anti-body against pre-synaptic voltage gated Ca channels c. anti-body against Ach receptors |
a. ALS
b. Lambert-Eaton myasthenic syndrome c. Myasthenia Gravis |
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What is the cause of Lambert-Eaton myasthenic syndrome?
Clinical presentation? Treatment? |
a. autoimmune response against pre-synaptic Ca channels which does not allow vescicles to fuse so Ach never released to post synaptic receptors.
b. muscle weakness but after repeated use less weak, sometimes they have lung cancer c. repeated muscle use increases Ca accumulation in terminal and increases Ach release |
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What causes Myasthenia gravis?
What is the clinical presentation? Treatment? |
a. autoimmune has Abs against the Ach receptor causing ligand gated channels on end plate to decrease
b. muscle weakness due to lack of ability to contract c. treated with Acetylcholinesterase inhibitors so that Ach stays around and channels open longer |
