Proprioceptors Flashcards
What are proprioceptors and where are they found?
somatosensory receptors that are found in the muscles, tendons and joints.
What is the structure of a muscle spindle?
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.
Which motor neurone innervates the muscle spindle?
Gamma MN
Describe the mechanism of simple control of posture (contraction)
- Muscle contracting too little to overcome gravity
- Spindle stretched, increasing afferent activity
- Increased excitation of the motor neurone pool
- Increased force of attraction
What are the differences between the centre and ends of intrafusal muscle fibres?
Centres are passive, elastic structures whereas the ends are contractile and change length at the same time as the main muscle (extrafusal)
What happens to the afferents when the central regions are stretched?
They depolarise
When is the muscle spindle afferent activated, during muscle stretch or during muscle contraction?
Muscle stretch
Activation of the gamma MN causes muscle contraction: true or false?
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).
Describe the general mechanism of inhibiton
- Muscle stretches as part of a voluntary movement
- Descending control systems activate inhibitory interneurones
- Reduced activity in the motor neurone pool
- Muscle doesn’t resist stretching
Describe reciprocal inhibition
1a afferents excite interneurones that directly inhibit antagonist motor neurones.
These interneurones are glycinergic - act through ligand-gated receptors on the motor neurone itself.
Describe presynaptic inhibition
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 (GABAb) on axon terminals.
What is the main difference between the results of presynaptic and reciprocal inhibiton?
Presynaptic = slow onset, long lasting, powerful
Reciprocal = rapid onset, short lasting, weak
Which motor neurone does a lower motor neurone refer to?
alpha-motor neurone
What are the effects of lower motor neurone lesions?
Denervate the muscle -> flaccid paralysis :
- weakness
- wasting
- loss of reflexes
- fasiculations + fibrilations
What does an upper motor neurone do?
Carries signals from the brain to the spinal motor circuits, control alpha + amma motor neurones, control inhibitory interneurones too
Where can an upper motor neurone lesion be found?
Anywhere between the cell body (brain) and lower motor neurone
What effect will upper motor neurone lesions have?
- 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)
Which afferents are ‘nuclear bag’ and ‘nuclear chain’ fibres associated with?
Nuclear bag = type Ia
Nuclear chain = type II
What do group II afferents encode for?
Sensitive to length of muscle
What are some characteristics of group II afferents?
- 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
What can loss of upper motor neurone input to group II reflexes cause? How is it treated?
Hypertonia - treated by suppressing group II reflex, eg. tizanidine (acts via a2 receptors to suppress activity in interneurones)
What do group Ia afferents encode for?
Sensitive to rate/velocity of stretch
What are some characteristics of group Ia afferents?
- thicker, faster axons
- monosynaptic connections to a-MNs
- respond to rate of change in length
- important for correcting rapid unintended movements
What can loss of upper motor neurone input to group Ia reflexes cause? How is it treated?
Spasticity - need to damp down group Ia reflex, eg.
- > boost effectiveness of GABAa receptors so benzodiazepines
- > more specific, activate GABAb receptors - baclofen
Which sensory afferent fibre is associated with golgi tendons?
1b
What do golgi tendons sense?
Active muscle tension
What are the two pathways controlling strength of muscle contraction activated by GTO? What controls it?
- Non reciprocal inhibition
- Excitatory interneurones
Upper motor neurones control which is active at any moment
Describe non-reciprocal inhibition of GTO and when it’s important and consequences of loss of it
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.
Describe excitatory pathways of GTO and when it’s important and the consequences of loss of it
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.
