Proprioceptors Flashcards

1
Q

How can the force of contraction be modified?

A
  • change the frequency of AP firing in the active motor units
  • change the number of active motor units
  • change the type of active motor units
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2
Q

What are the different types of motor units?

A
  • fast glycolytic, fast oxidative and slow oxidative
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3
Q

Fast glycolytic

A
  • Glycolytic produce very fast, powerful twitches, but are harder to excite enough to reach threshold. Have large motor units so will have lots of muscle fibres that they can contract simultaneously
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4
Q

Slow/fast oxidative

A
  • slow oxidative are very small units and so will have less fibres contracting simultaneously - therefore are more easily excited and so are recruited first
  • We excite the smallest motor units we can, until we need more power, so we excite more and recruit the bigger units.
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5
Q

Muscle spindles and control

A
  • when we hold our arm up, muscle spindles fire to keep the arm stable and avoid drooping
  • muscle spindles are stretch receptors - as soon as the muscle starts to stretch, its afferent activity is increased, excites motor neurone and increase force of contraction
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6
Q

What MN axons are in control of gamma motor control?

A
  • Alpha MN axons control surrounding fibres
  • Gamma MN axons contract the poles of the intrafusal fibres
  • activated and deactivated simultaneously to keep the central portion unaffected by movement - stopping it from firing
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7
Q

Gamma motor control - moving our arm

A
  • muscle stretches as part of voluntary movement
  • intrafusal centres dont stretch, so afferent activity unchanged
  • no excitation of MN pool
  • muscle doesn’t resist stretching
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8
Q

Gamma motor control - picking up object heavier than exprected

A
  • muscle will be under more load than expected
  • muscle shortens too slowly
  • intrafusal poles are not under load, so they shorten as intended
  • intrafusal centres stretch increasing the afferent acitivity
  • increases the excitation of the MN pool
  • increased force of contraction corrects the movement
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9
Q

Gamma motor control - inhibition

A
  • muscle stretches
  • descending control systems activate inhibitory interneurons
  • reduces the activity of the motor neurone pool
  • muscle doesnt resist the stretching
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10
Q

What is reciprocal inihibition?

A
  • if we activate a muscle spindle arc on one muscle, it will deactivate the antagonist muscle
  • e.g. if we use biceps, the triceps will be inhibited
  • 1a afferents from biceps muscle will excite inhibitory interneurons going to the triceps motor neurons
  • these interneurones are glycinergic - allow Cl- to flow into the cells and hyperpolarise them
  • rapid in onset, short-lasting, relatively weak
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11
Q

What is presynaptic inhibition?

A
  • not inhibiting by hyperpolarising the MN, it inhibits the effectiveness of muscle spindle reflex arc
  • 1a afferents excite interneurons that inhibit release of NT from anatagonist 1a afferents
  • GABAergic interneurons - GABAb receptors on axon terminals
  • slow in onset, long-lasting and powerful
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12
Q

Lower motor neurone lesions

A
  • In skeletal muscle, the LMN is the alpha-motor neurone.
  • lesion can be anywhere in the spinal cord or severed axons in the nerve
  • Denervated some or all of the muscle fibres - cannot be told to contract, causing them to waste and turn to connective tissue
  • get weakness of the muscle - tested by getting someone to press against you
  • lose reflex movements
  • fasiculations and fibrillations
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13
Q

Upper motor neuron lesions

A
  • can have a UMN lesion anywhere from the brain to the spinal segment you are looking at
  • most important is corticospinal tract
  • if you sever these or destroy bodies, you no longer get a control signal from the brain
  • UMNs intiaiate and control movement via a-MNs/y-MNs - lesions will stop this working - get muscle weakness
  • also switch on inhibition to allow muscle to move via inhib. interneurons - lesions cause increased muscle tone and increased reflexes (completely under control of reflex arc)
  • muscle paralysed but still contracting - no muscle wasting
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14
Q

What are the different classes of intrafusal muscle fibres?

A
  • Nuclear bag fibres - type 1a afferents

- nuclear chain fibres - type 2 afferents

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15
Q

Type 2 afferents

A
  • tell the brain about the length of the muscle
  • thinner, slower muscles
  • mainly indirect connection to aMNs
  • important for maintaing limb position, posture and resting muscle tone
  • loss of UMN input to type2 = hypertonia (can be treated by supressing type 2 reflex, Tizanidine - a2-antagonist)
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16
Q

Type 1a afferent

A
  • AP potential doesnt corellate to length, it responds to the speed of its stretch (faster the stretch, the more activity)
  • Thicker, faster axons
  • monosynaptic connection to aMNs
  • important for correcting rapid unintended movements
  • test - tap tendon
  • loss of UMN input to 1a reflexes causes velocity-dependent increase in tone (spasticity)
  • treat by dampening down 1a reflex - spinal inhibition boosting effectiveness of GABAa receptors (BZDs) or mimicking presynaptic inhibition, acitivating GABAb receptors (Baclofen - better)
17
Q

Golgi tendon organs

A
  • the end of a muscle - tendon is made of collagen fibres.
  • 1b afferent (fat, fast) has sensitive endings that wind between collagen fibres in encapsulated area of tendon
  • If collagen fibres are stretched out, they squash the endings which causes AP firing.
  • respond to active tension by muscle itself when it contracts
18
Q

GTO - controlling muscle tension (STATIC)

A
  • Afferents activate inhib. interneurone.
  • Non-reciprocal inhibition as it goes back to the same muscle
  • Interneuron is glycinergic
  • Prevents the muscle tone from rising beyond what is needed - keep you standing upright but need no more than that
  • Loss of GTO driven inhibition causes hypertonia in static situations
19
Q

GTO - controlling muscle tension (DYNAMIC)

A
  • Enable excitatiory interneurone
  • used to boost muscle contraction at key points in the gait cycle
  • loss of GTO driven excitation will cause weakness in dynamic situations (don’t get the boost of excitation they need)