Proprioceptors

Question 1

What are proprioceptors and where are they found?

Answer 1

somatosensory receptors that are found in the muscles, tendons and joints.

Question 2

What is the structure of a muscle spindle?

Answer 2

Small sensory organs enclosed in a capsule. They have contractile proteins (thick and thin filaments) at either end. The central region is wrapped by sensory dendrites. They are found in parallel with extrafusal fibres.

Question 3

Which motor neurone innervates the muscle spindle?

Answer 3

Gamma MN

Question 4

Describe the mechanism of simple control of posture (contraction)

Answer 4

1. Muscle contracting too little to overcome gravity
2. Spindle stretched, increasing afferent activity
3. Increased excitation of the motor neurone pool
4. Increased force of attraction

Question 5

What are the differences between the centre and ends of intrafusal muscle fibres?

Answer 5

Centres are passive, elastic structures whereas the ends are contractile and change length at the same time as the main muscle (extrafusal)

Question 6

What happens to the afferents when the central regions are stretched?

Answer 6

They depolarise

Question 7

When is the muscle spindle afferent activated, during muscle stretch or during muscle contraction?

Answer 7

Muscle stretch

Question 8

Activation of the gamma MN causes muscle contraction: true or false?

Answer 8

False. The gamma MN activates contraction of the intrafusal fibers, which do not produce enough force to have any effect on the muscle as a whole. It is the alpha MNs that innervate the typical muscle fibers (extrafusal fibers) that produce contractions. Because of alpha-gamma coactivation, activation of the gamma motor neuron will occur at the same time as contraction of the muscle (but it doesn’t cause the contraction).

Question 9

Describe the general mechanism of inhibiton

Answer 9

1. Muscle stretches as part of a voluntary movement
2. Descending control systems activate inhibitory interneurones
3. Reduced activity in the motor neurone pool
4. Muscle doesn’t resist stretching

Question 10

Describe reciprocal inhibition

Answer 10

1a afferents excite interneurones that directly inhibit antagonist motor neurones.

These interneurones are glycinergic - act through ligand-gated receptors on the motor neurone itself.

Question 11

Describe presynaptic inhibition

Answer 11

1a afferents excite interneurones that inhibit release of NT from antagonist 1a afferents (so triceps to biceps).

These interneurones are GABAergic, act through metabotropic receptors (GABA_b) on axon terminals.

Question 12

What is the main difference between the results of presynaptic and reciprocal inhibiton?

Answer 12

Presynaptic = slow onset, long lasting, powerful

Reciprocal = rapid onset, short lasting, weak

Question 13

Which motor neurone does a lower motor neurone refer to?

Answer 13

alpha-motor neurone

Question 14

What are the effects of lower motor neurone lesions?

Answer 14

Denervate the muscle -> flaccid paralysis :

• weakness
• wasting
• loss of reflexes
• fasiculations + fibrilations

Question 15

What does an upper motor neurone do?

Answer 15

Carries signals from the brain to the spinal motor circuits, control alpha + amma motor neurones, control inhibitory interneurones too

Question 16

Where can an upper motor neurone lesion be found?

Answer 16

Anywhere between the cell body (brain) and lower motor neurone

Question 17

What effect will upper motor neurone lesions have?

Answer 17

• weakness (brain can’t tell muscle to contract)
• increased muscle tone + reflexes (brain can’t control reflex arcs)
• no wasting (muscles remain active due to reflex input)

Question 18

Which afferents are ‘nuclear bag’ and ‘nuclear chain’ fibres associated with?

Answer 18

Nuclear bag = type Ia

Nuclear chain = type II

Question 19

What do group II afferents encode for?

Answer 19

Sensitive to length of muscle

Question 20

What are some characteristics of group II afferents?

Answer 20

• thinner, slower axons
• mainly indirect connection to a-MNs
• respond in proportion to length of muscle
• important for maintaining limb position + posture + for resting muscle tone

Question 21

What can loss of upper motor neurone input to group II reflexes cause? How is it treated?

Answer 21

Hypertonia - treated by suppressing group II reflex, eg. tizanidine (acts via a2 receptors to suppress activity in interneurones)

Question 22

What do group Ia afferents encode for?

Answer 22

Sensitive to rate/velocity of stretch

Question 23

What are some characteristics of group Ia afferents?

Answer 23

• thicker, faster axons
• monosynaptic connections to a-MNs
• respond to rate of change in length
• important for correcting rapid unintended movements

Question 24

What can loss of upper motor neurone input to group Ia reflexes cause? How is it treated?

Answer 24

Spasticity - need to damp down group Ia reflex, eg.

• > boost effectiveness of GABA_a receptors so benzodiazepines
• > more specific, activate GABA_b receptors - baclofen

Question 25

Which sensory afferent fibre is associated with golgi tendons?

Answer 25

1b

Question 26

What do golgi tendons sense?

Answer 26

Active muscle tension

Question 27

What are the two pathways controlling strength of muscle contraction activated by GTO? What controls it?

Answer 27

1. Non reciprocal inhibition 2. Excitatory interneurones Upper motor neurones control which is active at any moment

Question 28

Describe non-reciprocal inhibition of GTO and when it's important and consequences of loss of it

Answer 28

Afferents activate an inhibitory interneurone, the interneurone is glycinergic Prevents muscle tone from rising beyond what is needed, useful in static situations (eg. standing). Loss of GTO driven inhibition will cause hypertonia in static situations.

Question 29

Describe excitatory pathways of GTO and when it's important and the consequences of loss of it

Answer 29

In dynamic situations (eg walking), a pathway via an excitatory interneurone is enabled. Used to boost muscle contraction at key points in gait cycle. Loss of GTO driven excitation will cause weakness in dynamic situs.