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Flashcards

Proprioceptors

Hannah Tribe Neuro Degree English 40 cards

Cards in this deck (40)

  1. 1If muscle twitching is an all-or-nothing event, how is force of muscle contraction modified? (3)1. Change the frequency of firing of APs to the active motor units
    2. change the number of active motor units
    3. Change the type of active motor units (e.g. red to white)
  2. 2Which motor units are recruited most easily and why?'red' motor units, as these consist of the red muscle fibres which are more easily excited, but produce only a small, weak twitch
  3. 3Which are the last to be recruited?Large motor units consisting of white muscle fibres, as these require the largest excitatory input
  4. 4How is posture controlled?Stretch-sensitive afferent neurons detect stretches of muscle fibres that are away from the desired point, and cause increased firing of APs to the spinal cord, where it causes the reflex action of increased stimulation of the motor neuron to that muscle, to increase its contraction.
  5. 5So how do we voluntarily stretch our muscles?If the brain is signalling the efferent motor fibres to move, then both alpha and gamma motor neurons are contracting/relaxing at the same time and rate, because the end poles of gamma MNs are just as contractile as the alpha MNs. This synchronicity means that the central portion of the intrafusal muscle fibre, where the proprioceptor afferents are, does not change its length and therefore does not stimulate the reflex that would cause contraction of the muscle.
  6. 6How can gamma motor control ensure the accuracy of movement?When the alpha and gamma MNs become out of sync (e.g. when an object is heavy and the alpha MNs are contracting too slowly but gamma MNs are contracting normally [because it is the alpha MNs that support the weight of objects]), the intrafusal muscle fibre central portions become stretched and so stimulate the proprioceptor reflex, which stimulates increased force of contraction of the muscles. It is the reflex way of making the alpha MNs 'keep up' with the gamma MNs.
  7. 7How does reciprocal inhibition work?The proprioceptor afferents branch not only into the part which synapses directly onto the motor neuron which causes the contraction of the muscle, but also to a part which synapses onto an interneuron which synapses with the motor neuron to the antagonist muscle to give an inhibitory signal and force the antagonist muscle to relax
  8. 8How do the interneurons inhibit the motor neuron of the antagonist muscle?the interneurons are glycinergic and so glycine binds to ligand gated Cl- channels on the motor neuron allowing influx of Cl- and therefore hyperpolarisation of the cell, making it harder to excite.
  9. 9What are 3 characteristics of reciprocal inhibition?1. Rapid onset
    2. Relatively weak
    3. Short-lasting
  10. 10What other interneuron does the 1a afferent synapse with?A GABAergic interneuron which synapses directly (via GABAb metabotropic receptors) onto the terminal of the 1a afferents of the antagonist muscles and inhibits the release of the neurotransmitter from the pre-synaptic terminal. This effectively 'switches off' the reflex arc of the antagonist muscle.
  11. 11What are 3 characteristics of presynaptic inhibition?1. Slow onset
    2. Longer-lasting
    3. More powerful
  12. 12What is a lower motor neuron?In skeletal muscle, these are the alpha MNs, which connect the spinal cord to the muscle itself
  13. 13What are the effects of a lesion of a LMN? (4)The innervation to the muscle itself has been totally lost, so there will be:
    1. Weakness
    2. Muscle wasting
    3. Arreflexia
    4. Fasciculations/Fibrillations
  14. 14What is an upper motor neuron?The neuron from the brains motor cortex down to the level of the spinal cord (mostly by the corticospinal tract) where it will synapse with the LMN.
  15. 15What do UMNs do? (3)1. Control alpha MNs
    2. Control gamma MNs
    3. Control inhibitory interneurons
  16. 16What are the effects of an UMN lesion? (3)1. Weakness (because the brain cannot tell the muscle to contract voluntarily)
    2. Increased muscle tone and reflexes, because reflex arc is still intact and therefore there is spontaneous contraction of the muscles
    3. No muscle wasting, as muscles are still active due to intact reflex arc.
  17. 17What are the 2 main types of intrafusal muscle fibres, and which afferents are they associated with?1. Nuclear bag, associated with type Ia afferents
    2. Nuclear chain, associated with type II afferents
  18. 18What do type II afferents do?They are slower due to their slower, thinner axons, but are responsible for maintaining limb position, posture and resting muscle tone over longer periods of time. They synapse with excitatory interneurons, which then synapse with the motor neuron.
  19. 19What is the result of loss of upper motor neuron input to group II afferents?Hypertonia
  20. 20How can this be reduced?By suppressing the group II reflex. Alpha-2 agonists and L-DOPA have been shown to help.
  21. 21What do group Ia afferents respond to?The velocity of the movement (rate of change of length of muscle fibre)
  22. 22Which afferents respond to illiciting reflexes with a tendon hammer?Group Ia
  23. 23What is the result of loss of upper motor neuron input to group Ia reflexes?Spasticity (velocity-sensitive hypertonia)
  24. 24What are treatment options for spasticity?1. General increase in spinal inhibition (lowering the reflex), by giving GABAa receptor agonists, benzodiazepines
    2. GABAb agonists which will cause presynaptic inhibition of the Ia reflex which is causing the spasticity, such as baclofen
  25. 25What are 1b sensory afferents?These are fibres which originate within a capsule, would round collagen fibres in the tendons of muscles.
  26. 26How are the fibres arranged and how does this help its function?The nerve endings are would between the collagen fibres so that when the muscle is stretched and the collagen fibres become taut, is compresses the nerve endings and causes them to fire APs
  27. 27What is this system called?The Golgi tendon organ
  28. 28What do they measure and respond to?Tension generated by active muscle contraction
  29. 29What are the 2 afferent pathways in the Golgi tendon organ?Excitatory and inhibitory
  30. 30What decides which is active at any time?Upper motor neurons
  31. 31Which pathways is active during standing still?The inhibitory pathway, where a glycinergic inhibitory interneuron is activated and prevents muscle tone getting too high.
  32. 32Which type of inhibition is this?Non-reciprocal
  33. 33During dynamic situations (e.g. walking), which pathway is activated and what effect does this have?The excitatory pathway is activated, and this boosts muscle contraction via positive feedback during certain times of the gait cycle
  34. 34If GTO inhibition is lost, what is the result?Hypertonia while static
  35. 35If GTO excitation is lost, what will happen?Weakness during dynamic situations
  36. 36What is an example of a protective reflex?The flexor/ withdrawal reflex causes limb withdrawal on a painful cutaneous stimulus, and is polysynaptic. This also works with the crossed extensor reflex, which causes contralateral limb extension, so your weight leans on the other limb.
  37. 37What is a central pattern generator?This is where groups of interneurons are recruited to perform a stereotyped movement as a reflex after it has been consciously activated, such as walking.
  38. 38Why do UMN lesions cause clonus?There is conflict between the opposing muscle groups, so there is jerking movement between the two.
  39. 39What is pyramidal weakness?Fixed flexion in the arms due to these muscles being stronger than the extensors, and the opposite in the legs as the extensors are stronger.
  40. 40Why do LMN lesions cause hypotonia?There no longer a balance between the stretch reflexes of opposing muscle groups, so the muscles have no tone.

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Degree Neuro Flashcards on Proprioceptors, created by Hannah Tribe on 16/11/2014.
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Hannah Tribe
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proprioceptorsneuronsnervous systemmotor neurons
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