Test #3 Flashcards

1
Q

Movement of our muscles is controlled at two levels in the CNS:

A

1) circuitry within the spinal cord allows for coordinated control of movement
2) these circuitry mechanisms can be modified by descending input from the brain

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2
Q

Motor Control can be divided into

A

1) spinal cord regulation and control of coordinate muscle contraction
2) brains regulation and control of spinal cord circuitry

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3
Q

What are the 3 basic types of muscles? Difference between each one?

A

Cardiac, Skeletal, and Smooth.
Cardiac + Skeletal are striated.
Cardiac is unique in that cells exhibit automatism, innervation by the ANS serves to increase or decrease rate of contraction

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4
Q

What kind of control is the somatic motor system? How does the CNS control contraction?

A

Somatic is voluntary.

CNS controls contraction by varying fire rate or motor neurons and recruiting additional synergistic motor untis

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5
Q

Describe the structure of the muscle.

What kind of tissue is on each structure?

A

Each muscle is made up of fascicle, and each fascicle is made up of several muscle fibers, and each fiber is made up of several myofibrils.
Each muscle is wrapped by epimysium, each fascicle is wrapped by perimysium, and each fiber is wrapped by endomysium

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6
Q

How does extension and flexion work?

A

antagonistic muscles working in opposite directions, that is, when one muscle contracts, another relaxes. Flexion at the elbow requires coordinated contraction

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7
Q

How are muscles controlled? Name the two types

A

By lower motor neurons only! Higher motor neruons only exert indirect control over muscles.

1) Alpha Motor neurons (associated with muscle contraction)
2) Gamma motor neurons (associated wihth intrafusal fibers)

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8
Q

Difference between Alpha motor neurons and Gamma

A

Alpha innvervate extrafusal fibers and Gamma innvervate intrafusal fibers

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9
Q

What is a motor unit? Name the two types

A

Defined as an alpha motor neuron and all the muscle fibers it innervates.
Fast motor units (white fibers, rapidly contract and fatigue)
Slow motor units (dark fibers, slow to contract and slow to fatigue)
Each motor unit innervates only one type of muscle fiber

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10
Q

Name the 3 sources of input to the alpha motor neuron

A

Sensory info from muscle spindles.
Upper motor neurons in motor cortex and brain stem
Interneurons in spinal cord

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11
Q

How does muscle contraction occur?

A

When ACh binds to nicotinic ACh receptors. This causes a change in muscle membrane potential that in turn triggers release of Ca sarcoplasmic reticulum surrounding the myofibrils. This increase in calcium causes the thin filaments to bind to and move along the myosin filaments pulling Z lines toward one another

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12
Q

Explain the sequence of muscle contraction

A

(excitation)
1. An AP arrives at the presynaptic terminal and ACh is released into the synaptic cleft causing opening of ligand-gated channels on the sarcolemma and influx of Na ions, which brings depolarization.
2) Depolarization results in AP that spreads throughout the sarcolemma and into the system of T tubules.
3) Ca ionsarereleased into the sarcoplasm from the sarcoplasmic reticulum.
(contraction)
4. Ca ions bind to troponin exposing myosin binding site
5. The myosin head now attaches to actin, the myosin head pivots and ADP is released.
(relxation)
6. The attached myosin head binds ATP, and the myosin head detaches.
7. ATPase hydrolyzes the newly bound ATP, and the cycle continues as long as ATP and Ca ions are present

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13
Q

Where is feedback for the muscles located?

A

By proprioceptors in the muscle. Muscle spindls provide info about muscle length. These fibers are innervated by gamma motor neurons. Golgi Tendon Organs provide info about muscle tension

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14
Q

List the diseases affecting muscular movement

A

Amyotrophic Lateral Scelerosis involves the degeneration or loss of alpha motor neurons.
Muscle Dystrophy involves muscle degeneration over time due to a defective gene that codes the protein for dystrophy.
Myasthenia Gravis involves the production of antibodies that bind to bodys own nicotinic ACh receptors, interfering with norml neuromuscular transmission

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