Neuromotor system Flashcards
Structure of muscle
- whole muscle (organ)
- Muscle fibre (composed of myofibrils)
- Cytoskeletal components of myofibrils
- Protein components of myrofibrils
- myosin (thick filaments)
- actin (thin filaments)
- troponin
- tropomyosin
Feature of neuromuscular synapse
Largest synapse in the body, excitable synapse, can undergo reinnervation if damaged
Total failure diseases of neuromuscular junction
MND - death of alpha motor neurons
Spinal Muscular Atrophy - defect in SM1 gene necessary for survival of motor neurons
Total failure diseases of the neuromuscular junction
- Motor neurone disease - the death of lower motor neurons
Spinal muscular atrophy - SMN1 gene defect which is required for motor neuron survival
The function of skeletal muscle
Generates heat, Movement, vocalisation, posture
Steps of muscular action potential
The generation of motor neuron action potential at the axon initial segment This action potential then skips down the motor axon to the motor nerve terminal . This motor action potential will then open up voltage gated calcium channels that allows for an influx of calcium ions into the motor nerve terminal. This causes synaptic vesicles which contain the neurotransmitter acetylcholine to fuse with the presynaptic membrane of the motor nerve terminal, at specialised sites called active zones. The neurotransmitter then leaves the nerve terminal to bind to acetylcholine receptors, which are ligand gated ion channels. Once the acetylcholine binds to its acetylcholine receptor sodium ions flow into the muscle. This causes a in the local membrane potential called an excitatory postsynaptic potential, which then further opens up sodium voltage gated channels. This together brings the membrane potential of the muscle to threshold to induce a muscle action potential. This then leads to excitation contraction coupling and muscle contraction.
Partial failure diseases of the neuromuscular junction
- produce some action potentials but not enough to get a strong enough contraction presenting with muscle weakness or slowness of movement
- Lamberts syndrome (Presynaptic error): antibodies remove voltage gated ion channels. Not enough calcium -> not enough neurotransmitter release -> not reaching threshold to generate action potential
- Myasthenia Gravis (postsynaptic error): loss of ACH receptors-> great neurotransmitter release but not enough receptors to drive opening of sodium gated ion channels to cause action potential
Possible solution get rid of enzyme that gets rid of ACH so there is constant supply so that even though there is limited receptors there is enough neurotransmitter to generate action potential
Latency period
delay between generation of action potential and generation of muscle force
Motor unit
1 motor neuron to a number of muscle fibres
Fibre grouping
Fibre grouping occurs when a motor neuron dies, typically the large type 2b as they are more susceptible. Then the muscle fibres are reinnervated by a new motor neuron nearby, a small motor unit. This reinnervation determine the muscle types so they become type 1 twitch fibres. Even though this brings back motor fibres they aren’t as strong as they initially were as type 2b meaning overall the muscle strength is decreased and creates fibre type grouping of slow fibres
Functions of muscle spindles, golgi tendons and joint receptors (Purpose of gamma motor neurons )
Muscle spindles - muscle length (nuclear chain fibres) and velocity of contraction (nuclear bag fibres)
- Muscle spindles innervated by gamma motor neurons simultaneous with alpha motor neurons innervating muscle. This allows the muscle spindles to record muscle contractions by contracting simultaneously
Golgi tendon - muscle tension
- Located in tendinous insertions, Golgi tendons are intertwined in collagen fibres so when they contract the Golgi tendon is pinched signalling muscle tension
Joint receptors (Ruffini) - joint position
Reciprocal inhibition
sensory information comes in and innervates the motor neuron to go to the muscle. This sensory path burificates to innervate an inhibitory interneuron to act upon antagonistic muscle at the same time as the leg is lifting the sensory information from the muscle spindles is sent to also act upon the antagonistic muscle. However due to the inhibitory interneuron it is unable to reach threshold and a movement isn’t triggered
Stretch reflex enhanced
Reflex can be enhanced by convergence when a sensory stimulation enters the spinal cord diverges, one of its pathways excitation the local motor neuron and the other traveling to the brain and synapsing there. This synapse triggers another excitation of some local muscle from the brain enhancing the reflex due to innervation from two sources
Feedforward and feedback
Feed forward - anticipates a loss of posture
Feedback -when posture is lost to produce rapid corrective response
Postural adjustment
Muscles closer to point of disturbance activated first
Deep cerebellar nuclei
Deep cerebral nuclei are innervated by the purkinje fibres which have and inhibitory affect.
Innervations from mossy fibres (motor) and climbing fibres (sensory) are having an affect on the deep cerebellar nuclei but also send axons to innervate the purkinje neurons to turn on and off their inhibitory function to allow modulation of postsynaptic neuron. Mossy fibers inhibit the purkinje fibres and climbing fibres excitate
