NeuroMotor Flashcards

1
Q

What are direct and indirect connects

A

There are direct and indirect pathways onto the motor neuron that determine the out put activity.

Direct can be seen as alpha motor neurons while indirect can be noted as interneurons.

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2
Q

What are Betz cells

A

Upper motor neurons are present in the cerebral cortex where they synapse at the spinal cord.

Travel down the spinal cord via corticospinal tracts.

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3
Q

Key roles of skeletal muscle

A
  • Movement
  • Maintain posture
  • Stabilizes joints
  • Generates heat (core body temp determined by muscle mass)
  • Lymphatic drainage
  • Venous return
  • Vision Reproduction
  • Digestion
  • Excretion
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4
Q

Why are there folds at the neuromuscular junction

A

Note the folds present at the neuromuscular junction, this allows the AcH receptors to be very close to the alpha motor neuron facilitating a fast synapse. However it allows for more voltage gated Na channels causing a faster transition from resting membrane potential and threshold.

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5
Q

What are active zones at the motor terminal

A

AcH is release upon calcium entry at these active zones

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6
Q

What type of receptor does AcH bind to at the motor endplate

A

Ligand gated ion channels

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7
Q

Diseases that will causes total failure of the neuromuscular synapse

A

Total failure of the neuromuscular synapse leads to muscle paralysis which can result in death due to respiratory failure

  • Motor neuron disease - 80% die 3-5 yr post due to resp failure. Death of lower motor neurons
  • Spinal muscular atrophy (SMA) - autosomal recessive disease caused by a defect in a SPECIFIC gene (SMN1). The SMN1 gene is vital in survival of alpha motor neurons
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8
Q

What is the result of partial failure of the neuromuscular junction and where does this occur.

A

Causes muscle weakness which may be due to inability to recruit enough larger motor units for strong muscle contractions. Causes defects in either the motor nerve terminal or in the region of muscle below the motor nerve ending known as the post synaptic region. Both have the same result of muscle weakness.

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9
Q

Process of AP generation at the neuromuscular junction

A
  1. AP arrives at motor nerve terminal triggering the opening of VGCC at the active zones and subsequent entry of Ca+
  2. Calcium causes the release of AcH from synaptic vesicles at the active zones
  3. AcH travels the synaptic cleft to bind to the ligand gated ion channels which causes large Na movement in and small K out.
  4. Results in local depolarisation which creates a current flow with the adjacent membrane of the muscle causing Na influx at this adjacent segment.
  5. Causes a rise in membrane potential to threshold triggering an AP
  6. ACh is destroy via the enzyme Acetylcholinesterase
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10
Q

2 examples of disease causing partial failure at the neuromuscular junction

A
  • Defects in the motor nerve terminal (Lambert Eaton Syndrome) -auto immune disease effecting the pre synaptic voltage gated calcium channels resulting in poor neurotransmitter release → muscle weakness
  • Defects in the muscle’s post synaptic region (Myasthenia Gravis) - Causes a decrease in the post synaptic AcH receptors causing the frequency of muscle APs to drop → weakness
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11
Q

What are muscular dystrophies

A

Muscular dystrophies → Duchenne’s Muscular dystrophies cause muscle weakness due to a mutation in the dystrophin gene (none).

This means that during eccentric contractions the membrane can be damaged causing calcium to flow out and proteases to flow in.

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12
Q

Two ways in which the neuromuscular system grades the force of contraction

A

The neuromuscular system grades the force of contraction in two main ways, rate modulation and motor unit recruitment.

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13
Q

What is rate modulation

A

frequency in which muscle APs can be generated

Single AP generates short twitch so to generate larger contraction multiple APs need to arrive from MU in close succession. This will result in twitch summation. This will eventually reach a point known tetanus.

This is only relevant for SINGLE muscle fiber tension. Whole muscle tension needs this as well as motor unit recruitment.

Different MUs have different firing properties.

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14
Q

What is the safety factor at the neuromuscular junction

A

The neuromuscular synapses has a safety factor, there are more AcH receptors than will ever be used meaning that regardless of the amount of neurotransmitters that is release an excitatory response can always cause an AP.

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15
Q

What is a motor unit

A

1 motor neuron and all of the muscle fibres it innervates

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16
Q

What is a motor neuron pool

A

All the available motor units for a specific muscle

17
Q

Size and control trade off in MUs

A

Large motor units can elicit more force however they have decreased control.

18
Q

What is motor unit recruitment

A

The activation of additional motor units to achieve an increases in the contractile strength (tension of the whole muscle).

19
Q

What is Hennemans size principle

A

For a given synaptic input MU recruited from smallest to largest (cell body size). This result in successive contraction of slow twitch muscle fibres to fast twitch as contraction increases.

Fibre type 1 → 2a → 2B

Therefore need to increase synaptic drive for larger MU recruitment.

20
Q

Mechanism behind the size principle

A

Smaller MU have high membrane resistance and require lower depolarizing current to reach threshold.

Important to note that the larger motor units will still register the EPSP but it is not sufficient to get it to threshold

21
Q

What is fibre type grouping

A

With age there is chronic deinnervation and then subsequent reinnervation leading to a type 1 dominance

Fibres loose connections with MN death, form new connections. The larger MUs hae increased metabolic load and therefore stress causing them to die first.

22
Q

How does neural activity determine fibre type

A

Amplitude and duration of Ca in muscle will determine type of myosin that is used. Therefore short duration but higher amplitude (type 2b like contraction) will use a different type of myosin and pathway than a long duration and low amplitude (type 1 like contraction)

23
Q

What components make up a spinal cord reflex

A

Consists of MNs (A and G), interneurons and afferents

24
Q

Neurotransmitters at the spinal cord

A

Excitatory -AcH and glutamate

Inhibitory - glycine

25
Q

3 types of neural circuits with examples

A

Post synaptic gaiting

Also referred to as reciprocal inhibition

Afferent input to spinal cord which will split into 2 excitatory alpha motor neurons to the flex/ext. There is also an inhibitory interneuron hyperpolarising the flexor group. This means that although there is an excitatory input to the flexor group due to the hyperpolarisation from the interneuron an AP isn’t created.

Convergence

Presence of an upper motor neuron will further excite an output.

Enhance reflex by thinking about it

Divergence

Step one stone and one leg flexes will other extends.

Example is crossed extensor coupled with the withdrawal reflex.

26
Q

2 types of muscle spindles

A
  • Nuclear chain fibres (length)

Continual sensory input about muscle length

Nuclei in a chain

  • Nuclear bag fibres (velocity of contraction)

Rate of change of muscle length

Along the chain there is a bulge (bag)

27
Q

Why are muscle spindles innervated by G MN

A

They have a motor innervation so that the muscle spindles can contract in time with the extrafusal muscle fibres to ensure they can constantly read tension. This occurs through a gamma motor neurons allowing the spindle to maintain sensitivity during muscle contraction. Conc muscle will conc spindle to ensure information from 1a sensory fibre.

28
Q

4 brain stem motor centres and explanation

A
  • Reticular formation - gets info from pre motor centers and coordinates lower motor neuron pools. Related to more complex movements, both ipsilateral and bilateral tracts.
  • Red nucleus - role in motor learning
  • Superior colliculus - Integrator. Gets many inputs for integration and relates to eye traction as well as head and neck reflexes
  • Vestibular nucelli - align head with gravity, gets info from vestibular regarding positions of the head
29
Q

Vestibular nuclei and their function

A

Lateral vestibular nuclei - motor neurons for extensor muscles (maintaining stance) via lateral vestibular tract

Superior and medial vestibular nuclei - motor neurons for extraocular muscles of the eye. Coordination of eyes with head movements via medial vest tract

Inferior - integrates afferents and cerebellum to higher centers

30
Q

2 mechanisms for postural adjustment

A
  • Feedforward - compensatory reflexes. Rapid, stereotyped and show a space time organisation
  • Feedback - anticipatory reflexes. Pre programmed, not reflex like and are altered with experiences. Modify motor behaviour before.
31
Q

Motor cortical regions and their functions

A

Primary motor cortex:

  • Controls simple features of movement on opposite side of the body
  • Split into motor homunculus where areas that need more fine control (face) have smaller MUs but increased number.

Supplementary motor area:

  • Thinking about movement, active during movement visualisation
  • Functions by planning integrated skilled movements
  • Output to primary motor cortex (70%) and spinal cord (30%)
  • Located at dorsal midline, anterior to PMC

Premotor cortex:

  • Anterior to PMC
  • Get ready
  • Plans integrated skill movements, hands and mouth
  • Close to Broca’s area (speech)
  • Output to SMA and PMC