Physiology Flashcards

1
Q

What is the main role of dendrites in the neuron?

A
  • Receive inputs from other neurones

- Give graded electrical signals to the soma

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2
Q

What is the main role of the cell body/soma of a neuron?

A
  • Contains nucleus, ribosomes, mitochondria and endoplasmic reticulum (ER)
  • Integrates incoming electrical signals that are passed to the axon hillock
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3
Q

What is the main role of the axon hillock/ initial segment?

A

site of initiation of the ‘all or none’ Action Potential (AP)

as all info has been integrated together by this point

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4
Q

What is the function of the axon?

A
  • conducts output signals as APs to the presynaptic terminal.
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5
Q

What type of signal generates a positive change in membrane potential that could generate an AP?

A

Excitatory/ depolarixing stimulus

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6
Q

What type of signal prevents an AP from being generated?

A

Inhibitory stimulus (causes membrane to hyperpolarize - aka get more negative)

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7
Q

How are neurons classified based on neurite number?

A

Unipolar (one neurite)
Pseudounipolar (one neurite that immediately bifurcates)
Bipolar (two neurites)
Multipolar (multiple neurites)

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8
Q

Give an example of each type of neuron classified by neurite number

A
Unipolar = peripheral autonomic neuron
Pseudounipolar = dorsal root ganglion neuron
Bipolar = retina
Multipolar = lower motor neuron
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9
Q

What are the 4 functional regions of neurons?

A

Input - what stimulates them (i.e. another neuron?)
Integrative - where all info is integrated (cell body)
Conductile - where integrated info is transmitted (axon)
Output - where nerve ending acts upon (secretions/ muscle/ other neuron)

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10
Q

What ion is responsible for the upstroke and downstroke in an action potential?

A
Upstroke = Na+ influx
Downstroke = K+ efflux

these do NOT happen in sync, hence the up and down strokes

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11
Q

What is a projection neuron and how does this compare to an interneurone?

A

Projection = from one region of brain to another (e.g. cortex -> thalamus

Interneurone = found in particular areas of brain, integrate info and change it to suit this part of brain before it is passed to projection neuron

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12
Q

Why does the downstroke occur when the membrane potential reaches +40mV?

A

This is the equilibrium point of Na+

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13
Q

Why is there a brief period of undershoot where the membrane hyperpolarises, before it returns to a stable resting potential?

A

The membrane permeability to Na and K is constantly changing and therefore hasn’t quite settled by the time the downstroke reaches resting membrane potential

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14
Q

Why do passive signals at the peripheral terminal of the neuron not spread far from their site of origin?

A

They are not as strong as an AP therefore will diminish

ALSO - neurons are leaky and current is lost across the membrane

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15
Q

What factors within a neuron can be altered to promote faster conduction?

A

Increased membrane resistance (less leakage)

Decreased axial resistance of the axoplasm (current comes across no obstacles inside neuron)

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16
Q

How can membrane resistance be increased?

A

Myelinate axons

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17
Q

What is meant by Saltatory Conduction?

A

action potential ‘jumps’ from one node of Ranvier to the next for faster conduction

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18
Q

What conditions cause demyelination?

A
multiple sclerosis (CNS)
Guillian-Barré syndrome (PNS
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19
Q

Briefly explain how APs cause release of neurotransmitter at a synapse

A
  • Depolarization by AP
  • Ca2+ influx
  • Ca2+- induced release of transmitter (exocytosis from vesicles)
  • Receptor activation on post synaptic membrane
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20
Q

How is neurotransmitter removed from the synaptic cleft before the next AP?

A
  • Enzyme inactivation of transmitter

- Reuptake of transmitter into presynaptic neuron

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21
Q

Drugs which block enzymes from inactivating neurotransmitter in the synaptic cleft are used in what conditions?

A

Alzheimers

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22
Q

Where can an axon from the pre-synaptic neurone meet the post-synaptic neurone?

A

Dendrite (Axodendritic) VERY COMMON
Soma (Axosomatic) COMMON
Axon (Axoaxonic) UNCOMMON

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23
Q

What neurotransmitter is commonly released in the CNS by an excitatory signal?

A

Glutamate

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24
Q

What effect does glutamate have on post-synaptic receptors?

A
Activates ionotropic receptors
Allows cations (+ve Na+, K+, Ca2+) into neuron
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25
Q

What neurotransmitter is released in the CNS in response to an inhibitory signal?

A

Gamma-aminobutyric acid (GABA)

OR Glycine

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26
Q

What is the difference between spatial and temporal summation of action potentials?

A

Spatial summation = Many presynaptic neurones release neurotransmitter to create one AP

Temporal summation = single neuron may release all the neurotransmitter for one AP

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27
Q

What are the main groups of substances used as neurotransmitters?

A

Amino acids (e.g. glutamate)
Amines (DopAMINE)
Peptides (cholecystokinin)

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28
Q

What is the difference in speed of transmission in Ligand Gated Ion Channel receptors and G-Protein coupled receptors?

A

Ionotropic ligand-gated ion channels mediate FAST neurotransmission

G-Protein Coupled Receptors mediate slow neurotransmission

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29
Q

Describe the structure of ionotropic LGIC receptors vs that of metabotropic receptors

A

Ionotropic receptor for neurotransmitter is ITSELF a CHANNEL

Metabotropic receptors bind neurotransmitter and then signal to other G Proteins etc to open a channel to let ions in

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30
Q

If glutamate has both ionotropic and metabotropic receptors on the post-synaptic membrane, what kind of respons does this create?

A

A fast and slow EPSP are generated from each of the channels respectively

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31
Q

What types of ionotropic receptors can Glutamate bind to and activate an ion channel?

A

AMPA
Kainic Acid
collectively non-NMDA

NMDA

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32
Q

How do the responses of each ionotropic glutamate receptor differ?

A

AMPA - large but transient AP

NMDA - smaller and slower AP

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33
Q

What sensations are picked up by the somatosensory system?

A
  • Fine discriminatory touch [light touch, pressure, vibration, stretch]
  • Joint and muscle position sense (proprioception)
  • Temperature (thermosensation)
  • Pain (nociception)
  • Itch (pruriception)
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34
Q

What are the 3 divisions of the somatosensory system classified by where the sensation comes from?

A

Exteroceptive division (cutaneous senses => skin)

Proprioceptive division (muscle, tendons and joints)

Enteroceptive division (viscera and autonomic function)

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35
Q

How may neurons are usually found in series in a somatosensory pathway?

A

3

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36
Q

What parts of the 1st order sensory neuron are known collectively as a SENSORY UNIT?

A

Receptor, cell body and axon

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37
Q

Where are the 1st, 2nd and 3rd order neurones normally found?

A
1st = dorsal root ganglia /cranial ganglia 
2nd = dorsal horn of spinal cord/ brainstem nuclei
3rd = thalamus
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38
Q

Describe how sensory stimulation at the peripheral terminal of the 1st order neuron creates an AP

A
  • Stimulus (mechanical, thermal, or chemical)
  • Opens cation channels
  • Depolarizes receptor potential
  • If over threshold triggers AP
  • AP frequency goes up if membrane is depolarized more
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39
Q

Explain what is meant by the Adaptation rate of sensory units

A

Does the unit APs fire continuously or does it respond preferentially to a changing stimulus?

E.g. When going from brightly lit area to dim room, eyes take a while to adapt due to stimulus change

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40
Q

What is the stimulus of fine touch and what sensory unit does it act upon?

A

Stimulus: mechanical force on skin

Sensory unit: skin mechanoreceptors

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41
Q

What stimulates proprioception and what snesory unit does it act upon?

A

Stimulus: Mechanical forces acting on joint and muscles

Sensory Unit: Joint/ Muscle Mechanoreceptors

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42
Q

What sensory units detect changes in temperature?

A

Thermoreceptors

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43
Q

What are the potential stimuli that can induce pain in nociceptors?

A

Strong mechanical force on skin/viscera

Heat on skin, mucous membranes, viscera

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44
Q

What stimulates sensation of an itch at pruriceptors?

A

irritant (e.g. chemical) on skin or mucous membranes

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45
Q

What type of threshold unit responds to non-damaging stimuli?

A

Low threshold units

  • fine discriminatory touch
  • cold -> hot temperatures
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46
Q

What type of threshold unit responds to noxious and potentially damaging stimuli?

A

High threshold units

nociceptors, mechanoreceptors, thermal nociceptors and chemical nociceptors

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47
Q

Describe AP conduction in a Slowly adapting (SA) or tonic/static response

A

Continuous APs to CNS for entire length of stimulus

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48
Q

Describe AP conduction in a Fast adapting (FA) or phasic/dynamic response

A
  • Detects changes in stimulus strength

- Number of impulses increases when rate of change of stimulus increases

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49
Q

Describe AP conduction in a Very fast adapting (very FA) or very phasic/dynamic response

A
  • Responds only to very fast movement, such as rapid vibration
  • One AP generated at beginning of mechanical stimulus
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50
Q

Which types of axon have the highest and lowest conduction velocities?

A

A-Alpha = highest (80-120ms-1)
**due to high axon diameter and myelin sheath

C = Lowest (0.5-2.0ms-1)
** due to no myelination and small axon diameter

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51
Q

What is a receptive field?

A

target territory from which ONE sensory unit can be excited

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52
Q

Areas of skin with small receptive fields have high acuity. TRUE/FALSE?

A

TRUE

skin on the fingertips = small receptive fields due to high innervation density

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53
Q

Where are pacinian corpuscles found and what sensation do they mediate?

A

FOUND: Dermis or subcutaneous fat

SENSATION: Vibration (mediated by capsule around nerve ending)

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54
Q

What do Ruffini nerve endings mediate?

A

Strong mechanical pain

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55
Q

What sensation do Meissner’s corpuscles mediate and where are they found?

A

FOUND: Dermo-epidermal junction

SENSATION: touch (contributes to texture)

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56
Q

Merkel disks consist of a sensory axon and a merkel cell. What are the functions of these?

A

Sensitive to light touch

Merkel cells make neurotransmitter for sensory nerve terminal

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57
Q

Where are Krause end bulbs found and what do they mediate?

A

FOUND: border of dry skin and mucous membranes
SENSATION: touch

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58
Q

What sesnation can the root hair plexus detect?

A

Movement of hair in a particular direction

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59
Q

How can low threshold mechanoreceptors be classified?

A

Slow or Fast adapting? (SA or FA)
Small or large receptive field? (1 or 2)
=> SA1 or FA2 is a “physiological subclass” of an A-alpha receptor

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60
Q

Low threshold mechanoreceptors comprise of a receptor and what else?

A

A “Parent fibre type”

e.g. A-alpha, A-beta etc

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61
Q

Encapsulated nerve ending mechanoreceptors (e.g. meissners corpuscles, pacinian corpuscles, ruffini endings) have what parent fibre type?

A

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62
Q

What Low threshold mechanoreceptors are associated with Aβ fibres?

A
  • Follicular nerve endings
  • Merkel cell-neurite complexes
  • Encapsulated nerve endings
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63
Q

What parent fibres are associated with free nerve endings?

A

Aδ, or C
=> thin or no myelination
=> SLOW

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64
Q

Describe the difference in receptive field for pacinian corspuscles and meissner’s corspuscles

A
  • Pacinian corpuscles = Large RF
  • There is an area of MAX. sensitivity
  • BUT corpuscle responds when the stimulus is strong enough anywhere within RF
  • Meissner’s corpuscle = Small RF
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65
Q

What frequencies are pacinian and meissner’s corspuscles most likely to pick up?

A
Pacinian = 200Hz
Meissners = 50Hz
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66
Q

Meissner’s corpuscles need the vibration to be indented further into the skin than pacinian corpuscles before becoming activated. TRUE/FALSE?

A

TRUE

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67
Q

If a single dorsal root is cut, why does the corresponding dermatome not lose all sensation?

A
  • degree of overlap with the region of adjacent dorsal roots
  • Therefore if T4 dorsal root was damaged, there would still be sensation in T4. To lose ALL sensation T4,5,6 would need to be damaged
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68
Q

What virus lies latent until reactivated in a dermatomal distribution?

A

Shingles

Lies in dorsal root ganglia until reactivated

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69
Q

Describe the changes in grey and white matter as you move up the spinal cord, and why this change is required?

A

More white matter and less grey matter as you move up from sacral -> cervical.

This is due to more afferent fibres joining further up and more white matter is needed to carry all these axons

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70
Q

How is the grey matter in the ventral and dorsal horns of the spinal cord divided?

A

Divided into 10 laminae of Rexed

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71
Q

What laminae are found in the dorsal horn and what afferent signals terminate here?

A

I and II most posterior in dorsal horn
- nociceptors found here

III to VI found in anterior of dorsal horn
- Low threshold mechanoceptors found here

VII to IX in ventral horn
- Proprioceptors found here

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72
Q

Using the Dorsal Column/Medial leminiscus tract and the Spinothalamic tract, explain what symptoms a patient with Brown-Sequard syndrome would experience if there was hemisection of the spinal cord.

A

Dorsal Column/ML Tract = touch, vibration
=> This would be lost on the ipsilateral side of the hemisection, as sensory input doesnt cross until brainstem

Spinothalamic Tract = Pain, temp
=> This would be lost on the contralateral side to the hemisection, as the sensory fibres cross segmentally in this tract

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73
Q

What are the two sections of the dorsal column called and what levels do they extend to/from in the spinal cord?

A

Gracile = Medial section
- extends whole way up spinal cord

Cuneate = Lateral section
- extends from T6 upwards (to deal with info from upper limbs)

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74
Q

What can the dorsal column/medial leminiscus pathway be used for?

A
  • Stereognosis – recognise an object by feeling it
  • Vibration
  • Fine touch (two point discrimination)
  • Conscious proprioception – awareness of body position and movements
  • Weight discrimination
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75
Q

What is lateral inhibition and why/where does it occur?

A
  • Active neurone inhibits the activity of its neighbours via stimulating inhibitory interneurons lateral to it
  • This sharpens stimulus perception (eliminates background noise)
  • This happens in synapses of the DCML pathway
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76
Q

The DCML pathway does not exist for sensory information from the anterior head. What picks up this information instead?

A

Trigeminal divisions which feedback to the trigeminal ganglion and different nuclei in the brainstem

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77
Q

Where is the primary somatosensory cortex located?

A
  • Post central gyrus of the parietal cortex
    immediately posterior to the central sulcus (SI)
  • Adjacent to the posterior parietal cortex (SII)
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78
Q

What areas are found in the Primary somatosenspry cortex

A

Brodmann areas (BA) 1, 2, 3a and 3b

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79
Q

What areas of the primary somatosensory cortex receive most info from the thalamus?

A

Areas 3a and b receive around 70%

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80
Q

What sensations do each of the Brodmann areas deal with?

A

3a - proprioception
3b - Touch (texture, shape, size)
1 - Texture (as this receives input from 3b)
2 - Pressure and Joint position, distinguishing objects

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81
Q

Describe the organisation of the body parts in the primary somatosensory cortex

A

The toes are at the top of the post central gyrus with the tongue at the lower end, but the hand separates the head from the face

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82
Q

Describe the organisation of the columns in the sensory cortex

A

alternating columns of cells with rapidly adapting and slowly adapting sensory responses

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83
Q

Are each of the Brodmann areas using the same somatotopic map?

A

Yes - Adjacent strips of cortex have the same parts of the body in parallel to each other

BUT - maps are not identical, they are mirror images of each other

84
Q

An area of cortex responsible for a part of the body that has been amputated or damaged will be taken over by other parts of the body. TRUE/FALSE?

A

TRUE

areas next to it controlling other parts of the body will extend into the area

85
Q

What happens if the sensory input from a particular area of the body increases?

A
  • cortical space for that digit increases

relative to other inputs generating less activity

86
Q

Describe a condition where cortical remapping can become an issue

A

Phantom limb pain

If a limb is amputated and other parts of the body take over that area of cortex, a pain stimulation in these areas can cause the brain to feel it as pain from the non-existent limb

87
Q

What is the job of the posterior parietal cortex?

A

Receives and integrates information from SI and other cortical areas

  • (visual, auditory)
  • sub-cortical areas (thalamus)
88
Q

What condition can arise due to damage of the posterior parietal cortex?

A

Neglect syndrome

  • If damage is on RHS of posterior parietal cortex, then patients fail to acknowledge the left side of the world exists.
  • No vision problems, Patients just disclaim the existence of things, including their own left leg!
89
Q

The somatic motor system is responsible for what type of skeletal muscle movement?

A

Voluntary movement

And involuntary spinal reflexes

90
Q

What two neurons make up the somatic motor system?

A
  • upper motor neurones (UMNs) within the brain and

- lower motor neurones (LMNs) within the brainstem and ventral horn of the spinal cord

91
Q

What is the main function of upper motor neurons (UMNs) in relations to lower motor neurons (LMNs)?

A

upper motor neurones (UMNs) modulate the activity of Lower motor neurons (LMNs)

92
Q

LMNs receive input from UMNs and what other places?

A

proprioceptors and interneurons

93
Q

LMNs command the ‘final common pathway’. What is the function of this?

A

To cause muscle contraction

94
Q

What two types of muscle fibres are found in LMNs? One supplies the bulk of the muscle whilst the other supplies the muscle spindle.

A

alpha (α) motor neurones (α-MNs) - supply muscle bulk

Gamma (γ) motor neurones (γ-MNs) - supply spindle

95
Q

What is meant by “synergistic muscles” such as biceps brachii and brachioradialis?

A

They both aim to complete the same movement (i.e. arm flexion)

96
Q

What name is given to muscles which oppose each others action?

A

Antagonist

e.g. tricep is an antagonist of biceps brachii

97
Q

What is the difference between axial and distal muscles?

A

Axial muscles control movements of the trunk (posture)

Distal muscles move the hands, feet and digits (allowing fine manipulation of objects by the hand)

98
Q

Why are the ventral horns of the spinal cord larger at the cervical and lumbar enlargements?

A

More alpha motor neurons are found here for relay of motor info to the upper and lower limbs

99
Q

What is encompassed in a motor unit?

A

α-MN and all of the skeletal muscle fibres that it innervates

100
Q

What name is given to all of the alpha motor neurons innervating one muscle?

A

motor neurone pool

101
Q

What does each AP cause in a muscle fibre?

A

A muscle twitch

Summation of twitches causes a sustained contraction

102
Q

Describe the somatotopic map of the ventral horn of the spinal cord?

A

Axial muscles = medial
Distal muscles = lateral
Flexor muscles = more dorsal in the ventral horn
Extensor muscles = anterior of ventral horn

103
Q

What 3 neurons can input to an alpha-motor neuron?

A
  • dorsal root ganglion cells
  • Upper Motor Neurons
  • Spinal interneurones
104
Q

Muscle force is dependent on what factors?

A
  • Firing rates of the LMNs
  • No. of LMNs that are all active (=> more motor units contributing)
  • Co-ordination of the movement (agonist versus antagonist)
  • Muscle fibre size (hypertrophy)
  • Fibre Phenotype (fast/slow)
105
Q

If the AP frequency is low, why does no prolonged contraction occur?

A

Enough time is given for the muscle to relax

“relaxation phase” involves calcium reuptake into the sarcoplasmic reticulum (SR) and the reversal of troponin cross-bridges

106
Q

Give an example of muscles in the body which require small motor units to carry out their function

A

extraocular eye muscles as fine movements are required

107
Q

Give an example of muscles in the body requiring large motor units to carry out their function?

A

large postural (antigravity) muscles e.g. leg muscles

108
Q

Motor units only contain fibres of one type i.e. fast or slow. TRUE/FALSE?

A

TRUE

slow and fast twitch fibres are interspersed throughout a full muscle but are specific in each individual motor unit

109
Q

Each muscle fibre is innervated by a single motor axon at endplate (neuromuscular junction). Where along the fibre are these found?

A

midway along the fibre, usually in the centre

110
Q

Why are muscle fibres divided into slow and fast twitch types?

A

They differ in how quickly myosin ATPase splits ATP

to provide energy for cross bridges

111
Q

What are the main types of slow and fast twitch muscle fibres?

A

Slow-oxidative (Type I)

Fast (Type IIa,IIb,IIx)

112
Q

What makes a muscle fibre Slow Type I?

A
  • Get ATP oxidative phosphorylation
  • Slow contraction and relaxation
  • Fatigue resistant.
  • Red fibres as high myoglobin content.
113
Q

What is the difference between Fast Twitch Type II muscle fibres?

A

IIa - ATP from oxidative phosphorylation

  • Fast contraction and relaxation
  • resistant to fatigue
  • well vascularised => relatively red in colour

IIb,IIx - ATP from glycolysis

  • fast contraction
  • NOT fatigue resistant
  • white in colour
114
Q

What is the Henneman size principle?

A

Smaller α-MNs (part of slow motor units) have a lower threshold => are recruited FIRST

THEN larger ones are recruited

=> LMNs are recruited in an order appropriate to the physical task that is being performed

115
Q

Describe the recruitment of LMNs from standing to running

A

Standing - Slow Type I
Walking - Fast Type IIa
Run - Fast Type IIx (IIb doesnt exist in many mammals including humans)

116
Q

Describe the Myotatic reflex

A

When a muscle is stretched, it pulls back

e.g. knee jerk response from quads

117
Q

What structure is responsible for the myotatic reflex?

A

Muscle spindle (sensory organ)

This is stretched with the muscle as it is parallel to the fibres

118
Q

What is found inside the fibrous capsule of the muscle spindle?

A
  • intrafusal muscle fibres

- sensory afferents (very fast conducting)

119
Q

Describe how the myotatic reflex is initiated?

A
  • Stretch of muscle spindle
  • Activation of Ia afferent (these are like Aα sensory fibres)
  • Excitatory synaptic transmission in spinal cord
  • Activate α-MN back to muscle
  • Contraction of muscle
120
Q

What manoeuvre can be attempted if a spinal reflex is deemed to be absent?

A

Jendrassik manoeuvre

  • patient interlocks fingers and tries to pull hands apart strongly when instructed
  • reflex is usually exaggerated
121
Q

What spinal levels are tested in the biceps, supinator, triceps, knee and ankle jerks?

A
Biceps C5/6
Supinator C5/6
Triceps C7
Knee L3/4
Ankle S1
122
Q

Why are α- and γ-MNs normally co-activated

to make the intrafusal muscle fibres in the muscle spindle contract in parallel with the extrafusal fibres?

A

To prevent the intrafusal muscle spindle fibres getting slack and not firing any APs

123
Q

What different named fibres are found in the muscle spindle?

A

Nuclear bag fibres:

  • Bag 1 or dynamic
  • Bag 2 or static

Chain fibres

124
Q

What sensory afferents wrap around the intrafusal fibres in the muscle spindle?

A

Ia afferents
- wind around the centre of all intrafusal fibres.

II fibres
- wrap around endings on all intrafusal fibres except the bag 1 dynamic type

125
Q

When are dynamic and static muscle fibres activated respectively?

A

Dynamic - γ-MNs are active when muscle length changes rapidly and unpredictably

Static - active when muscle length changes slowly and predictably only static γ-MNs

126
Q

Where are golgi tendon organs found and what are they involved in?

A

Found at junction of muscle and tendon

Involved in Inverse Myotatic Reflex

127
Q

Golgi tendon organs lie in series with muscle fibres rather than in parallel. TRUE/FALSE?

A

TRUE

128
Q

What is the function of the golgi tendon organs and the inverse myotatic reflex?

A
  • regulate muscle tension => protect muscle from overload
129
Q

Describe the neurone pathway in the reverse myotatic reflex?

A
  • Group Ib afferents (not Ia like in normal myotatic)
  • enter spinal cord
  • synapse upon INHIBITORY interneurones
  • these synapse upon the alpha motor neurones of the muscle to prevent contraction
130
Q

What types of nerve endings contribute to proprioception, and where are they found?

A
free nerve endings (in capsule and CT) 
Golgi-type endings (found only in ligaments)
Paciniform endings (found in periosteum)
Ruffini endings (found mainly in joint capsule)
131
Q

A loss of proprioception leads to what type of movement?

A

Vision guided movement

i.e. must look at limb before moving it OR must focus on an object in the distance to sit/stand without falling over

132
Q

What is meant by reciprocal inhibition?

A

The antagonist of a muscle must relax for the other to perform its function.
i.e. for the biceps to contract and flex the arm, the triceps must relax

133
Q

Excitatory interneurons mediate the flexor reflex and the crossed extensor reflex. Explain how these occur if a patient were to stand on a damaging stimulus, such as a drawing pin?

A
  • Sensory afferents detect damage by pin
  • Neuron sent back to spinal cord which diverges into 4 pathways
  • 1 excitatory pathway to flexor muscle and 1 inhibitory pathway to extensor muscle on AFFECTED side
  • 1 excitatory pathway to extensor muscle and inhibitory to flexor on OPPOSITE side (this is to provide stability whilst affected leg flexes upwards)
134
Q

What ion causes depolarisation to occur in the hair cells of the ear?

A

K+ influx from endolymph

135
Q

Explain how the hair cells cause sensory afferent signals to be produced?

A
Cilia move towards kinocilum 
K+ channels open due to tip link 
Hair cell depolarises
Ca2+ channels open
Vesicles of glutamate released to synapse with sensory afferent neuron
136
Q

More APs are generated when cilia move towards the kinocilum. TRUE/FALSE?

A

TRUE

137
Q

What are the ganglia of scarpa and where are they located?

A

Located in vestibular nerve just after CN VIII splits

- contain cell bodies of sensory neurons

138
Q

Explain how sound is produced and how we hear it

A
  • object (e.g. vocal cords) vibrate
  • air pressure changes
  • air vibrates in 3 dimensions towards ear
  • Causes eardrum, incus, malleus and stapes to vibrate
  • Stapes footplate vibration causes fluid in cochlea to move over hair cells
    => transduction
139
Q

What properties of the middle ear make it useful at amplifying sound?

A

Area ratio of tympanic membrane to stapes footplate = 20:1 => decreasing area over which the noise is exerted increases the pressure of the noise

Lever action of the ossicles (malleus higher than incus)
=> increases pressure of noise

Buckling of ear drum - middle is attached to malleus therefore moves less and preserves force

140
Q

What membrane separates the scala vestibuli and media?

A

Reissner’s membrane

141
Q

What membrane separates Scala Media and tympani?

A

Basilar membrane

142
Q

Which of scala vestibuli, media and tympani regress at the apex of the cochlea?

A

Media no longer exists

=> fluid in scala vestbibuli and tympani mix

143
Q

What is meant by the tonotopy of the basilar membrane?

A

particular spatial arrangement of frequencies detected

144
Q

The basilar membrane vibrates within the fluid of the cochlea. TRUE/FALSE?

A

TRUE

  • it is flexible and therefore can move with the fluid
  • It is widest and floppiest at the apex
145
Q

Do we have more inner or outer hair cells?

A

OUTER

15000-20000 compared to 3500 inner

146
Q

What is the role of the tectorial membrane?

A

vibrates and brushes against hair cells, making them move and release neurotransmitter

147
Q

What ganglion is located near the organ of corti, containing sensory neuron cell bodies?

A

Spiral ganglion

148
Q

Why must potassium be redistributed into the endolymph?

A

Causes problems such as deafness otherwise

=> mutations in any genes coding for K channels or transporters have the potential to cause deafness

149
Q

How do the outer hair cells amplify sound?

A
  • Have motor proteins on their sides which get compressed and change the length of the overall hair cell
  • this moves the basilar membrane more, and the inner cell moves with this membrane
  • inner hair cell then fires more sensory afferent transduction signals
150
Q

Describe the pathway from the cochlea to the primary auditory cortex

A

Cochlea -> cochlear nucleii -> superior olivary nuclei -> nucleus of lateral leminiscus -> Inferior colliculus -> Medial geniculate nucleus -> primary auditory cortex

151
Q

Which nuclei in the brainstem is important for the localisation of sound in space, and how does it do this?

A

Superior Olivary Nuclei

- senses time at which sound reaches each ear => intra-aural time difference

152
Q

What is the Calyx of Held?

A

Large nerve terminal ending with lots of vesicle active zones ready to discharge upon signal
- they usually react to High frequency sounds

153
Q

What 2 questions does the vestibular system function to answer?

A

1) Where am i going?

2) Which way is up?

154
Q

What do the semicircular canals sense?

A

Head angular acceleration (rotation)

155
Q

What do the utricle and saccule detect?

A

Head linear acceleration
saccule = vertical movement
utricle = horizontal movement

156
Q

Which of the semicircular canals share a plane?

A

Left anterior and Right posterior (and vice versa)

Both horizontal are also in the same plane

157
Q

What is the otoconia?

A

CaCO3 bio-crystals which help mechanical forces to reach the sensory hair cells in the utricle and saccule

158
Q

What are the 3 vestibular reflexes and what do they do?

A

Vestibulo-ocular - moves eyes in opposite direction of head moving so that vision remains still.

Vestibulo-colic - keeps head on level playing field when you walk

Vestibular-spinal - adjusts posture when rapidly changing position

159
Q

No input is needed from the motor cortex to rhythmically coordinate walking. TRUE/FALSE?

A

TRUE

Neuronal circuits causing flexion/extension of the legs can control this at spinal level

160
Q

Describe the 3 levels of motor control

A

Strategy – aim of the movement? How can it best be achieved?

Tactics – what sequence of muscle contractions and relaxations will fulfil the strategic aim?

Execution – activation of neurons which command the desired movement

161
Q

What areas of the brain are involved in producing a “strategy” for movement?

A

Neocortical association area and Basal Ganglia

162
Q

What areas of the brain are responsible for the “tactics” of a motor movement?

A

Motor cortex

Cerebellum

163
Q

What parts of the CNS cause execution of the planned movement?

A

Brain stem

Spinal cord

164
Q

What Brodmann areas make up the motor cortex in the pre-central gyrus?

A

Brodmann areas 4+6

165
Q

Name the two LATERAL descending motor tracts and their shared function

A

Lateral Corticospinal Tract + Rubrospinal Tract
Function:
- voluntary control of distal musculature
- particularly discrete, skilled, movements
- involved in fractionated movement (lots of different muscles making different movements at the same time)

166
Q

There are various ventromedial pathways which descend the brainstem. Name some examples and their main function.

A

Ventral Corticospinal
Tectospinal
Recticulospinal
Vestibulospinal

Function:
control of posture and locomotion

167
Q

The ventromedial pathways are under cerebral cortex control. TRUE/FALSE?

A

FALSE

The lateral pathways are under cerebral cortex control, whereas the ventromedial pathways are under brainstem control

168
Q

Where in the corticospinal tract does decussation of fibres occur?

A

Medullary pyramids

169
Q

Where do axons of the corticospinal tract terminate in the ventral horn of the spinal cord, and what muscles does this associate them with?

A

Terminate in dorsolateral region of the ventral horn

=> associated with distal muscles, particularly flexors

170
Q

Where are cell bodies of the rubrospinal tract located, and where does this nucleus receive input from?

A

Red nucleus

- receives input from the motor cortex and the cerebellum

171
Q

Where do fibres from the rubrospinal ract decussate?

A

decussate at the ventral tegmental decussation

172
Q

What muscles does the rubrospinal tract control?

A

Exerts control over limb flexor muscle

173
Q

If there is damage to only the Corticospinal tract, then the rubrospinal tract has the potential to compensate for the damage. TRUE/FALSE?

A

TRUE

174
Q

If both lateral tracts are damaged, explain the characteristics of patients movement?

A

Less fractionated
=> all muscles are trying to do same thing at same time
=> movement is larger and less accurate
=> also slower

175
Q

What are the two nuclei of the vestibulospinal tract?

A

Medial (goes to cervical region) and lateral ( goes to lumbar region)

176
Q

What is the function of signals descending via the lateral vestibular nucleus?

A
  • helps to hold upright and balance posture

- causes extension in antigravity muscles espeiclaly in lower limb

177
Q

What is the function of the medial vestibular nucleus

A
  • activate cervical spinal circuits (neck muscles etc)

=> guiding head movements

178
Q

Where are cell bodies of the tectospinal tract found?

A

superior colliculus

179
Q

Where does the superior colliculus receive input from?

A
  • retina
  • visual cortex
  • sensory and auditory afferents

=> e.g. helps to guide eyes to new important visual stimulus

180
Q

Where do axons of the tectospinal tract decussate?

A

Decussate in the dorsal tegmental decussation and descend close to the midline

181
Q

What are the two parts of the reticulospinal tract and where do they arise from?

A

Pontine (Medial) and Medullary (Lateral)

- arise from the reticular formation (diffuse mesh of neurones at the core of the brainstem)

182
Q

What are the functions of the Medial/Pontine Reticulospinal tract?

A
  • enhances antigravity reflexes of the spinal cord

- maintain standing posture by helping contract extensor muscles in the lower limbs

183
Q

What are the functions of the Lateral/Medullary Reticulospinal tract?

A
  • opposes the action of the medial tract

- releases antigravity muscles from reflex control

184
Q

Both of the reticulospinal tracts descend bilaterally. TRUE/FALSE?

A

FALSE
Medial/Pontine descends IPSILATERALLY
Lateral/Medullary decends BILATERALLY

185
Q

What are the three main types of pain?

A
  • nociceptive pain (immediate protective response, short-lived)
  • inflammatory pain (assists in healing, persists over days, possibly weeks)
  • pathological pain (no physiological purpose, persists over months -> years)
186
Q

Describe the difference in sensation of cutaneous, muscular and visceral pain

A
Skin = Well localised, pricking/stabbing
Muscle = Poorly localised, aching, tender, cramp,
Viscera = Poorly localised (referred to a somatic structure), dull, vague, associated with nausea
187
Q

What potential stimuli can activate nociceptors?

A

thermal, mechanical, chemical

188
Q

Nociceptors are 1st order neurons. TRUE/FALSE?

A

TRUE

Relay info to second order neurons in CNS

189
Q

What type of nerve fibres are nociceptors?

A

Aδ and C fibres

190
Q

Explain the difference in pain response from Aδ and C fibres

A

Aδ = respond to noxious mechanical and thermal stimuli
NOT CHEMICAL. Mediate ‘first’, or fast, pain

C fibres = respond to all noxious stimuli (e.g. they are polymodal). Mediate ‘second’, or slow pain as they wait for inflammatory mediators to activate them.

191
Q

Describe the difference in sensation between first “fast” pain from Aδ fibres and slow pain from C fibres.

A

First “fast” pain = stabbing, pricking sensations

Second “slow” pain = burning, throbbing, cramping, aching sensations

192
Q

What receptors can pick up noxious thermal stimuli?

A

members of the transient receptor potential (TRP) family: => TRPA1, TRPC3 and TRPV1

**TRPV1 also active at normal body temp, but when inflammation is present

193
Q

What receptors do noxious chemical stimuli activate?

A
H+ = Acid Sensing Ion Channels (ASICs)
ATP = P2X and P2Y receptors
Bradykinin = B2 receptors
194
Q

What temperatures activate Aδ Type I fibres?

A

Aδ Type I = 53 degrees

whereas Aδ Type II/ or C = 43 degrees

195
Q

What do efferent signals to nociceptor nerve endings cause?

A

Release of pro-inflammatory mediators

  • calcitonin gene-related peptide (CGRP)
  • substance P

These contribute to neurogenic inflammation

196
Q

What can noxious stimulation cause in the long term?

A
  • Increases spinal excitability
  • More efferent signals causing pro-inflammatory mediators at peripheral nerve terminal
    => can cause hyperalgesia (amplified pain)
    and allodynia (pain without a noxious input)
197
Q

Explain the synaptic connection between the 1st and 2nd order neuron in nociception.

A
  • AP opens voltage-gated Ca2+ channels
  • Ca2+ influx
  • Glutamate release from vesicles
  • Activation of glutamate receptors
  • Membrane depolarization (e.p.s.p.) (Mg2+ moves out of way in NDMA receptors)
  • Opening of voltage-gated Na+ channels
  • New AP
198
Q

Where in the dorsal horn of the spinal cord do Aδ and C fibres terminate?

A

Laminae of Rexed I and II
Laminae I contains Nociceptive specific (NS) cells which synapse only with C- and Aδ-fibres

  • then go on to interact with WDR neuron
199
Q

What other type of nerve fibre (aside from Aδ and C) terminates in the laminae of rexed and has input to the Wide dynamic range (WDR) neuron?

A

200
Q

Where does visceral pain come from?

A

Coverings of organs - e.g. pleura/peritoneum

When these are stretched/twisted/ischaemic = PAIN

NO PAIN if cut/burnt

201
Q

What nerve pathways are followed by visceral afferents from nociceptors before entering the dorsal horn of the spinal cord?

A

Follows sympathetic pathways

202
Q

What is viscerosomatic pain and how does it present?

A
  • sharp and well localised pain
  • occurs when inflammatory exudate from diseased organ contacts body wall structure
  • May present with diffuse visceral pain that progresses to sharp viscerosomatic pain (e.g. appendicitis)
203
Q

Pain evoked by activity in nociceptors (C- and Aδ- fibres) can be reduced by activity in Aβ-fibres. TRUE/FALSE?

A

TRUE - this details the “Gate Control Theory”

patients often find that focussing on low threshold activity involveing Aβ fibres distracts them from the pain

204
Q

What is the “Gate Control Theory”?

A

Firing of Aβ> Aδ and C fibres = GATE CLOSED

Firing of Aβ< Aδ and C fibres = GATE OPEN

if the gate is CLOSED then no 2nd order nociceptive signals fire to the brain

205
Q

How do Aβ fibres cause no projection from the 2nd order neuron?

A

They excite an inhibitory interneurone, which then inhibits the projection of any signal