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24 Cards in this Set
- Front
- Back
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Where are motor neuron cell bodies (for skeletal muscle) located in the spinal cord?
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anterior horn (sensory is in dorsal root ganglion/dorsal horn)
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What is the synaptic gutter?
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invaginations on the muscle membrane to increase surface area after the synaptic cleft
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What is the synaptic cleft?
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space between the neuron and the muscle it will innervate; neurotransmitters will travel through
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Acetylcholinesterase fucntion
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degrade acetylcholine
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Why are there many mitochondria in the axon terminal?
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ATP synthesis; ATP is needed to make acetylcholine in the neurons
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Once an action potential reaches a nerve, how are neurotransmitters released? (mechanism)
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action potential opens calcium channels > calcium rushes into the neuron from the synaptic cleft > calcium now in the neuron attract Ach vesicles to the dense bar/membrane > exocytosis
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Once Ach has been released into the synaptic cleft (neuromuscular junction), how does it elicit a response?
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binds to Ach receptors on muscle and opens ion gated channels. Sodium rushed into the cell (some K, Ca also). creates end plate potential that causes muscle contraction
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Assume Ach has bound to and opened a gated ion channel. Rank these ions by likelihood to pass through the channel (most likely to least likely): Ca, Cl, Na
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Na, Ca, Cl; Only + charged particles move through since the channel has - particles repelling - ions. Sodium has the highest gradient. Cl is - so it doesn't pass.
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What is the "end plate potential"?
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once sodium has rushed into the muscle (due to Ach opening the ion channels), the new electric potential of the muscle is higher (less negative). If this reaches the threshold (-40 mv), it will elicit a contraction
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Where is Acetylcholinesterase found?
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attached to the connective tissue of the synaptic cleft
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How does the poison "curare" work?
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competes with Ach to block the activation of gated channels = harder to reach the appropriate end plate potential to elicit muscle contraction
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How does the poison "botulin toxin" work?
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decreases Ach release by nerve terminals (vesicles don't migrate to the motor plate)
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How is there a safety factor for end plate potentials so that muscle contraction can occur even if there are some problems?
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the end plate potentials are usually 2-3x higher than they need to be (more Ach is released than is needed). so if there was a small problem, there wouldn't be an effect on contraction since the threshold would still be reached
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Where is Ach made?
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cytosol of nerve terminals, but is immediately stored in the vesicles
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Where do the vesicles (that will store neurotransmitters) come from?
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Golgi apparatus of the neuron
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Function of methacholine
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Ach agonist; but is not degraded by acetylcholinesterase. methacholine causes the gated channels to become leaky so muscles contract more > can lead to muscle spasms
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Function of neostigmine
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acetylcholinesterase inhibitor = raises levels of Ach available for muscle excitation
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What is myasthenia gravis?
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auto-immune disorder that attacks the Ach receptors. increasing levels of Ach are needed and achieved through acetylcholinesterase inhibitors
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Action potentials travel faster through (Muscles or Neurons)?
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neuron action potentials are 13 x times faster than muscle action potentials (myelination of neurons helps speed)
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Once Ach has stimulated the action potential in the muscle, how does the action potential spread to through the muscle?
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transverse tubules (T tubules) spread depolarization to the inner muscle cell to cause uniform contraction of muscle
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What is inside T tubules?
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Calcium in extracellular fluid. T tubules are connected to the extracellular compartment and run through the muscle cells (they are like very deep invaginations of the cell membrane)
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How does the T tubule release calcium? What causes the release?
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Since the T tubule is an invagination of the muscle cell membrane, it is depolarized when the rest of the muscle membrane is. The T tubules just carry the depolarization into the depths of the muscle fiber to ensure uniform contraction (called excitation-contraction coupling). T tubules contact the terminal cisternae of the sarcoplasmic reticulum and cause a release of calcium via DHT receptors
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Function of DHT receptors
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sense the action potential of the T tubule by detecting voltage change; then they cause releases of calcium from the sarcoplasmic reticulum for contraction
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After the muscle contraction occurs, what happens to the calcium in the muscle cytoplasm (sarcoplasm)?
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it is pumped back into the sarcoplasmic reticulum (ATP-dependent). can bind to calsequestrin in the SR
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