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PHASE ONE > Week 7 Neurology > Flashcards

Week 7 Neurology Flashcards

1
Q

What does the speed of propagation along a membrane depend on?

A

fibre diameter and myelination

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2
Q

The larger the fibre diameter …

A

the fast the action potential propagates, since larger diameter = less resistance to local current

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3
Q

Why does myelination increase propagation speeds?

A

There is less “leakage” of charge across the myelin meaning a local current can spread farther along an axon.
Also, the concentration of Na+ channels in the myelinated region of the axon is low. Therefore, action potentials only occur at the nodes of Ranvier, where myelin coating is interrupted and the concentration of voltage gated Na+ channels is higher.

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4
Q

What is the name for when action potentials jump between nodes of Ranvier?

A

saltatory conduction

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5
Q

What is the most common disease of the nervous system among young adults?

A

Multiple sclerosis

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6
Q

What is MS?

A

Degeneration of myelin and development of scar tissue which in turn disrupts and eventually blocks neurotransmission along myelinated axons

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7
Q

Symptoms of MS

A 
Uncontrolled eye movements/double vision
Slurred speech 
Partial/complete paralysis
Tremor
Loss of co-ordination 
Weakness
Sensory numbness, prickling, pain
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8
Q

Excitatory vs inhibitory synapse

A

The membrane potential of a post synaptic neurone is brought closer to threshold (Depolarised) at an excitatory synapse.
The membrane potential of a post synaptic neurone is either driven further from the threshold (hyper polarised) or stabilised at its resting potential at an inhibitory synapse.

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9
Q

2 types of synapse

A

Electrical

Chemical

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10
Q

Electrical synapse

A

The plasma membranes of the presynaptic and post synaptic cells are joined by GAP JUNCTIONS which allow local currents resulting in arriving APs to flow directly across the junction through connecting channels

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11
Q

Communication between nerve cells w electrical synapse SPEED

A

rapid

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12
Q

Chemical synapse

A

The plasma membranes of pre and post synaptic neurones are joined by the SYNAPTIC CLEFT
The synaptic cleft prevents direct propagation of the current from the presynaptic neurone. Instead, signals are transmitted across be means of NEUROTRANSMITTERS

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13
Q

Communication between nerve cells w electrical synapse SPEED

A

rapid

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14
Q

What do electrical synapses allow for?

A

synchronised transmission

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15
Q

Where are electrical synapses found

A

Brainstem neurones e.g. breathing and hypothalamus (hormone secretion)

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16
Q

What cells cover chemical synapses?

A

astrocytes (glial cells)

essential for the reuptake of excess neurotransmitter

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17
Q

Neurotransmitter release

A

Calcium ion channels open when an AP reaches presynaptic neurone.
Ca2+ ions cause vesicles containing neurotransmitters to move to release sites and fuse with presynaptic cell membrane and discharge their contents. Neurotransmitter diffuses across synaptic clef t and attaches to receptor sites.

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18
Q

5 processes of synaptic transmission

A
  1. Manufacture (intracellular biochemical process)
  2. Storage (vesicles)
  3. Release - AP
  4. Interact with post-synaptic receptors
  5. Inactivation
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19
Q

Where is ACh used?

A

In the brain and NMJs

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20
Q

2 main acetylcholine receptors

A

muscarinic

nicotinic

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21
Q

What happens once acetylcholine has been bound to the post-synaptic receptor?

A

acetylcholine esterase breaks it down into choline and acetyl
The choline can then be reabsorbed by the pre-synaptic neurone to be used to make more acetylcholine.

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22
Q

What can post synaptic neurone neurotransmitter receptors take the form of?

A

transmitter-gated ion channels

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23
Q

When NTs bind to the receptors/channels, it results in DEPOLARISATION or HYPERPOLARISATION depending on the channel type …

A

Depolarisation will occur in the excitatory channels and cause an excitatory post-synaptic potential EPSP where many Na+ leave and few K+ enter

Hyperpolarisation will occur in inhibitory channels (inhibitory post-synaptic potential IPSP) many K+ leave OR many Cl- enter

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24
Q

The combined effects of many excitatory synapses (since one event by itself is not enough to reach threshold) can be achieved by 2 means …

A
  1. TEMPORAL summation : input signals arrive from
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25
Q

The combined effects of many excitatory synapses (since one event by itself is not enough to reach threshold) can be achieved by 2 means …

A
  1. TEMPORAL summation : input signals arrive from the same presynaptic cell at different TIMES and summate since there are a greater number of open ion channels and thus a greater flow of positive ions into the cell.
  2. SPATIAL summation where 2 inputs occur at different locations in the PSN
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26
Q

Unbound neurotransmitters are removed from the synaptic cleft when …

A
  1. They are actively transported back into the presynaptic axon terminal (REUPTAKE) or by nearby glial cells
  2. They diffuse away from receptor site
  3. Are enzymatically transformed into inactive substances, some are transported back into the presynaptic neurone for REUSE
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27
Q

Fast neurotransmitters

A

Acetylcholine - ACh
Glutamate
GABA

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28
Q

What are neuromodulators?

A

Can cause change in synaptic membrane that last for longer time

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29
Q

What are neuromodulators associated with?

A

Slower events - learning, development, motivational states etc.

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30
Q

Neuromodulator examples

A

Dopamine
Noradrenalin
Norepenephrin
Serotonin

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31
Q

What are the most common local anaesthetics?

A

procaine

lignocaine

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32
Q

How do local anaesthetic work?

A

They interrupt axonal neurotransmission by blocking sodium channels thereby preventing the neurones from depolarising meaning that the threshold isn’t met and thus no action potential is developed to be propagated. This results in pain relief since pain isn’t transmitted.

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33
Q

How come local anaesthetics can work on muscles?

A

They can easily diffuse through mucus membranes thus can sometimes act on muscles too

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34
Q

What is the major neurotransmitter of the PNS at the neuromuscular junction ?

A

ACh (Also used in brain and spinal cord)

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35
Q

Neurones that release ACh are known as …

A

cholinergic neurons

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36
Q

ACh is synthesised from …

A

choline

acetyl coenzyme A in the cytoplasm of synaptic terminals and stored in synaptic vesicles

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37
Q

2 general types of ACh receptors

A

Nicotinic receptors (respond to nicotine as well)

Muscarinic receptors

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38
Q

Where are nicotinic receptors found?

A

In the neuromuscular junction

In the brain

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39
Q

Why are nicotinic receptors in the brain important?

A

They are important in cognitive functions and behaviour (attention, learning and memory - reinforces the ability to detect and respond to meaningful stimuli)

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40
Q

Why is tobacco so addictive?

A

There is presence of nicotinic receptors in reward pathways

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41
Q

Other than ACh, what do muscarinic receptors respond to?

A

mushroom poision muscarine

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42
Q

How do muscarinic receptors work?

A

They couple with G proteins, which in turn then alter the activity of a number of different enzymes and ion channels

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43
Q

Where are muscarinic receptors present?

A

brain and at junctions where a major division of the PNS innervates peripheral glands and organs, e.g. salivary glands and the heart and the lungs (bronchoconstriction)

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44
Q

Cigarettes contain nicotine with are agonists - what does this mean?

A

able to interact and open receptor

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45
Q

What inhibits the action of acetylcholinesterase? What does this cause?

A

Sarin
Build up of ACh in the synaptic cleft, resulting in an overstimulation of post synaptic ACh receptors, initially causing uncontrolled muscle contractions but eventually leading to receptor desensitisation and paralysis.

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46
Q

What neurotransmitter is found in the peripheral heart and CNS?

A

Noradrenaline

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47
Q

What is noradrenaline affected by?

A

Antidepressant drugs

  • Imipramine
  • Monamine oxidase

Stimulants
- Amphetamine

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48
Q

How does imipramine (AD drug) affect noradrenaline?

A

Blocks the reuptake of noradrenaline

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49
Q

How does monoamine oxidase (AD drug) affect noradrenaline?

A

inhibitor - increases the amount of noradrenaline by inhibiting the enzyme monoamine oxidase which is the enzyme used to break down noradrenaline

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50
Q

How does amphetamine affect noradrenaline?

A

increases release

blocks reuptake

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51
Q

What is an important transmitter in basal ganglia?

A

Dopamine

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52
Q

What is dopamine affected by?

A

Antipsychotic drugs (chlorpromazine)

Stimulants (amphetamine/cocaine)

Anti-parkinsons drug L-DOPA

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53
Q

How does chlorpromazine affect dopamine?

A

antagonist - blocks receptor so other neurotransmitter cannot activate receptor

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54
Q

How do stimulants affect dopamine?

A

Increase release

block reuptake

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55
Q

How does L-DOPA affect dopamine?

A

Increases dopamine manufacture

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56
Q

What effect does serotonin have?

A

An excitatory effect on pathways that mediate sensations

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57
Q

What is serotonin affected by?

A

Antidepressant drug - Prozac

Ecstasy

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58
Q

How does prozac affect serotonin?

A

SSRI - Selective serotonin reuptake inhibitor resulting in an increase in the concentration of synaptic serotonin

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59
Q

How does ecstasy affect serotonin?

A

Neurotoxic to serotonin neurone; destroy the terminal of axons

60
Q

What is the main excitatory NT?

A

Glutamate

61
Q

What is the main inhibitory NT?

A

GABA

62
Q

L-DOPA and Parkinson’s

A

In Parkinson’s there is a degradation/death of dopaminergic neurones
L-DOPA is a precursor for dopamine and is given to patients because it is able to cross the blood-brain barrier and is taken up by serotonin neurones and converted and released as dopamine because serotonin contains same enzyme needed to convert L-DOPA to dopamine as the dopaminergic neurones have.

63
Q

The axon terminals of a motor neurone contain vesicles similar to those found in synaptic junctions between 2 neurones. In NMJs, what is contained within these vesicles?

A

ACh

64
Q

What is a motor end plate?

A

The region of the muscle fibre plasma membrane that lies directly under the terminal portion of the axon

65
Q

What is a neuromuscular junction?

A

The junction of an axon terminal with the motor end plate is known as the neuromuscular junction

66
Q

When an action potential in a motor neurone arrives at the axon terminal …

A

it depolarises the plasma membrane, opening voltage gated Ca2+ channels and allowing Ca2+ ions to diffuse into the axon terminal from the ECF. The Ca2+ binds to proteins that enable the membranes of ACh containing molecules to fuse with the neuronal plasma membrane, thereby releasing ACh into the extracellular cleft, separating the axon terminal and the motor end plate.

67
Q

ACh diffuses from the axon terminal to the motor end plate where it binds to …

A

nicotinic receptor

68
Q

What is a key difference at the post synaptic part of NMJ?

A

The local depolarisation of the motor end plate, the END-PLATE POTENTIAL (EPP) has a much larger magnitude than an EPSP so one EPP is more than sufficient to depolarise the motor end plate to its threshold potential -> AP.

69
Q

The action potential is then propagated over the surface of the muscle fibres and into the …

A

T-Tubules

70
Q

What is the function of stretch receptors?

A

They monitor length and rate of change of muscle length

71
Q

What is a muscle spindle?

A

Stretch receptor consist of peripheral endings of afferent nerve fibres wrapped around modified muscle fibres - the entire apparatus is known as a muscle spindle.

72
Q

What is the name for modified muscle fibres within the spindle?

A

Intrafusal fibres

73
Q

What are the two ends of intrafusal fibres innervated by?

A

Gamma motor neurones (a type of lower motor neurone)

74
Q

Contractility of spindle

A

2 ends of muscle spindle are contractile, whilst central portion is non-contractile

75
Q

2 types of stretch receptor in the spindle

A

Nuclear chain fibres

Nuclear bag fibres

76
Q

What do nuclear chain fibres respond to?

A

How much muscle is stretched

77
Q

What do nuclear bag fibres respond to?

A

both the magnitude of stretch and the speed with which it occurs

78
Q

The middle 1/3rd of the spindle is associated with what kind of nerves?

A

Fast type 1a afferent sensory nerves

79
Q

The inferior and superior thirds of the muscle spindle are associated with what kind of nerves?

A

slow conducting type 2 afferent sensory afferents

80
Q

What slows down the rate of firing in the stretch receptor and what does this result in?

A

If action potentials along motor neurons cause the contraction of extrafusal fibres, the resulting shortening of the muscle removes tension on the spindle and thus slows the rate of firing in the stretch receptor, causing a reduction of sensory information.

81
Q

What is done to prevent the loss of sensory information from the contraction of extrafusal fibres?

A

Alpha-gamma coactivation
- the contractile ends of the intrafusal fibres are too small and weak to contribute to force or shortening of the entire muscle however they can maintain tension and stretch in the central receptor region thus activating the gamma neurones ALONE will increase the sensitivity of the muscle to stretch

Coactivating both the Alpha and Gamma motor neurones will prevent the central region of the muscle spindle from going slack during a shortening muscle contraction

82
Q

So what does alpha-gamma coactivation ensure?

A

that information about muscle length will be continuously available to provide for adjustment during ongoing actions and to plan and program future movements.

83
Q

What does tension depend on?

A

Muscle length, the load on the muscles, and the degree of muscle fatigue

84
Q

Why is feedback of muscle tension necessary?

A

to inform the motor control system of the tension actually achieved

85
Q

Golgi tendon organs - what do they monitor and measure?

A

Golgi tendon organs are receptors which specifically monitor how much tension the contracting motor units are exerting (or is being imposed on the muscle by external forces if the muscle is being stretched)
They measure the force developed by the muscles and any resultant change in length

86
Q

What are golgi tendon organs?

A

Endings of afferent fibres that wrap around collagen bundles in the tendons near their junction with the muscles

87
Q

What type of fibre leads from the golgi tendon organ to the spinal cord

A

1b fibres that run to the anterior horn of the spinal cord

88
Q

How are golgi tendon receptor endings activated?

A

When the muscle is stretched or the attached extrafusal muscle fibres contract, tension is exerted on the tendon - this tension straightens the collagen bundles and distorts the golgi tendon receptor endings thereby activating them.

89
Q

Branches of the afferent neurone (1b fibres) from the GTO cause the inhibition of …

A

alpha motor neurones of the contracting muscle, thereby inhibiting muscle contractions

90
Q

The output produced by the GTO is proportional to …

A

muscle tension

91
Q

What is a stretch or myotatic reflex crucial for?

A

control of muscle TONE

92
Q

Stretch reflex

A

Afferent fibres activate excitatory synapses directly on the motor neurones, which return to the muscle.

93
Q

Example of stretch reflex

A

Knee jerk reflex

94
Q

Knee jerk reflex

A

The patella tendon is tapped => the thigh muscles are stretched => stretch receptors are activated => burst of action potentials in the afferent nerve fibres => activate excitatory synapses on the motor neurones that control the muscle => extension of the lower leg

95
Q

What kind of arc is the knee jerk reflex?

A

Monosynaptic

96
Q

What kind of arc are other reflex arcs?

A

polysynaptic - they have at least one interneuron between the afferent and efferent neurone

97
Q

2 examples of polysynaptic reflex arcs

A

1 - RECIPROCAL INNERVATION - Afferent nerve fibres end on inhibitory interneurones; when activated these inhibit the motor neurones of the antagonistic muscle whos contraction would interfere with the reflex response (i.e. neurones that flex the knee would be inhibited)

2 - Motor neurones of synergistic muscles are activated i.e. other muscles that extend the leg

98
Q

Withdrawal reflex

A

Pain stimulation activates flexor muscles and inhibits extensor muscles, resulting in affected limb moving away from the harmful stimulus.

99
Q

Withdrawal reflex - legs

A

Where the legs are affected i.e. standing on a pin, the crossed-extensor reflex occurs simultaneously.
Where the motor neurons to the contralateral extensors are activated and the flexors are inhibited. This allows foe a shift in weight when the injured foot is lifted via flexion from the stimulus.

100
Q

Abnormally high muscle tone

A

Hypertonia

101
Q

When is hypertonia clearly seen?

A

When a joint is moved passively at high speeds - the increased resistance is due to an increased level of alpha motor neurone activity which keeps the muscle contracted despite the attempt to relax it

102
Q

Hypertonia usually occurs with disorders of the …

A

descending pathways which normally inhibit the motor neurones

Hypertonia indicates an UPPER MOTOR NEURONE DISORDER

103
Q

Alpha motor neurones are referred to as …

A

Lower motor neurones

104
Q

What is spasticity?

A

A form of hypertonia in which the muscles do not develop increased tone until they are stretched a bit, and after a brief increase in tone, the contraction subsides for a short time

105
Q

What is the Clasp-Knife phenomenon?

A

The period of ‘give’ occuring after a time of resistance with spasticity. When someone bends the limb of a patient; initially there is some resistance but after a certain point, resistance falls dramatically.

106
Q

What is the physiological cause of Clasp-Knife phenomenon?

A

1b afferent fibres from the Golgi Tendon Organs inhibiting alpha motor neurones once the GTOs detect tension; an example of the INVERSE STRETCH REFLEX

107
Q

The Clasp-Knife reflex is characteristic of…

A

Upper motor neurone lesion

108
Q

What is rigidity?

A

A form of hypertonia in which the increased muscle contraction is continual and the resistance to passive stretch is constant

109
Q

Hypotonia

A

low muscle tone
weakness
atrophy
decreased/absent reflex response

110
Q

Hypotonia might develop after …

A

cerebellar disease but also commonly accompanies disorders of the alpha motor neurones - LOWER MOTOR NEURONE LESION

111
Q

What are the most prominent nuclei of the basal ganglia?

A

Dorsal striatum: caudate nucleus and putamen

Ventral striatum: Nucleus Accumbens and olfactory tubercule

External globus pallidus
Internal globus pallidus

Substantia nigra

Subthalamic nucleus

112
Q

Which basal ganglia nuclei are rostral and which are caudal?

A

Rostral (upper) = striatum and globus pallidus

Caudal (lower) = substantia nigra and subthalamic nucleus

113
Q

Why does the substantia nigra appear black?

A

Neuramelanin that is produced as a by-product of dopamine production

114
Q

What is another name for the basal ganglia?

A

Corpus striatum

115
Q

What are the functions of the basal ganglia?

A

Connects inputs of the brain by recurrent loops

Facilitates purposeful behaviour and movement

Inhibits unwanted movement

Controls posture and movement

Selects which of the competing systems (emotions, cognitions and sensorimotor) to activate

116
Q

What type of output does the basal ganglia have?

A

Inhibitory

Tonically active

117
Q

Where is the primary motor cortex located?

A

Pre-central gyrus of the frontal lobe

118
Q

Direct pathway/Cortical loop e.g. in eye movement

A

The primary motor cortex sends excitatory messages to the striatum using GLUTAMATE. This excites the striatum resulting in it sending more inhibitory messages to the internal globus pallidus and the pars reticula of the substantia nigra using GABA. This inhibits the internal globus pallidus resulting in it sending LESS inhibitory messages to the thalamus. This also inhibits the pars reticulata meaning it sends less inhibitory messages to the pars compacta of the substantia nigra. This means the pars compacta is able to send more excitatory messages to further excite the inhibitory pathway to the pars reticulata thereby increasing the transmission of the direct pathway - using the neurotransmitter dopamine which binds to D1 Receptors. This also means the pars compacta inhibits the inhibitory pathway to the external globus pallidus from the putamen using dopamine which binds to D2 receptors, meaning the external globus pallidus is able to send inhibitory messages w/GABA to the subthalamic nucleus which inhibits the excitation of the pars reticulata (Which would result in no dopamine release). In addition, less inhibitory GABA messages are sent to the superior colliculus, meaning it is able to send more excitatory messages to the primary cortex using glutamate. Overall the thalamus is able to send more excitatory messages to the primary motor cortex and the combined effect of excitatory messages from the thalamus and superior colliculus to the primary motor cortex results in more eye movement.

119
Q

Indirect Pathway/Subcortical Loop (i.e. decreasing/stopping movement e.g. in eye movement)

A

The primary motor cortex sends an excitatory message to the PUTAMEN using glutamate. This causes the striatum to send more inhibitory messages to the external globus pallidus via GABA neurotransmitter. This inhibits the external globus pallidus meaning it is unable to inhibit the subthalamic nucleus. This means the subthalamic nucleus is able to send more excitatory messages to the internal globus pallidus and pars reticulata of the substantia nigra via glutamate. This excites the internal globus pallidus resulting in the release of inhibitory messages to the thalamus via GABA neurotransmitter. This excites the pars reticulata resulting in the release of inhibitory messages to the superior colliculus via GABA neurotransmitter. This inhibits the thalamus and superior colliculus meaning they are unable to excite the primary motor cortex resulting in no eye movement.

120
Q

Overview of Basal Ganglia disorders

A

Motor

  • Parkinson’s (lack of dopamine)
  • Huntington’s (lack of GABA)

Psychiatric disorders

  • Obsessive compulsive disorder (OCD)
  • Attention Deficit Hyperactivity Disorder (ADHD)

Secondary damage

  • Cerebral palsy
  • Wilson Disease
121
Q

What is the cause of Parkinson’s disease?

A

Not enough dopamine in the substantia nigra - loss of dopaminergic neurones
Less dopamine means that the external globus pallidus will not be able to inhibit the subthalamic nucleus meaning it will in turn excite the internal globus pallidus resulting in the inhibition of the thalamus and thus a DECREASE in movement.

122
Q

What are the symptoms of Parkinson’s?

A

Increased muscle tone - spasticity
Reduced movements
Bradykinesia (Slow movements)
-> problems doing up buttons, writing appears smaller, walking deteriorates (small steps and dragging of a foot)
- Tremor at rest and may be on one side only
- Muscle rigidity; pain

123
Q

Why does substantia nigra appear “faded” w Parkinson’s?

A

Less dopamine = less neuromelanin by-product (black pigment)

124
Q

Treatment of Parkinson’s

A

L-DOPA which can be used by serotonin neurones and converted to dopamine
(however dopaminergic neurones will continue to die)

Deep brain stimulation of the subthalamic nucleus which inhibits the subthalamic nucleus meaning the thalamus does not get inhibited and can thus excite the cortex resulting in improved movement

125
Q

What is Huntington’s?

A

Autosomal dominant disease with full penetrance. It is the result of too little GABA resulting in too much dopamine.

126
Q

What are the consequences of Huntington’s disease?

A

Decreased muscle tone
Overshooting movements
Dementia and personality change
Atrophy of ventricles in the brain result in the enlargement of the ventricles which in turn results in the destruction of the striatum (caudate nucleus and putamen; in particular the caudate)

127
Q

How is Huntington’s treated?

A

With dopamine receptor blockers

128
Q

What is the Limbic system essential for?

A

Adaptive behaviour, emotional responsiveness and the ability to learn new responses based on previous experiences (memory)

129
Q

2 main functions of the Limbic System

A

Learning

Regulation and translation of our emotional state into appropriate behaviour.

130
Q

The Limbic System consists of the …

A
  • cingulate gyrus
  • hippocampus
  • parahippocampal gyrus
  • anterior perforated substance
  • septal nuclei
  • uncus
  • amygdala
131
Q

Where is the limbic system located?

A

On the edge (limbus) of the hemisphere

132
Q

What is the brain’s ‘pleasure’ centre?

A

nucleus accumbens

133
Q

The various components of the limbic system are connected via the …

A

Papez circut

134
Q

What does the hypothalamus co-ordinate?

A

drive related behaviours through extensive connections in the brain as well as through the endocrine system

135
Q

Lesion of the anterior hypothalamus

A

inability to dissipate heat

136
Q

Lesion of the posterior hypothalamus

A

inability to retain heat

137
Q

Lesions of the lateral puberal nucleus (part of hypothalamus)

A

loss of hunger

138
Q

Lesions of the ventromedial nucleus (part of hypothalamus)

A

loss of satiety (feeling full)

139
Q

What does the removal of the hippocampus result in?

A

The inability to lay down new memories

140
Q

Where is working memory stored?

A

In the prefrontal cortex

141
Q

What is involved in the formation of new memories?

A

Mamillary bodies

142
Q

What different types of long term memory are there?

A

EXPLICIT memory (conscious memory e.g. remembering an appointment time) which can be EPISODIC (autobiographical) or SEMANTIC (knowledge about stuff)

IMPLICIT memory (unconscious memory e.g. sensory motor skills such as driving a car) which can be SKILLS/HABITS, CONDITIONED REFLEXES, EMOTIONAL

143
Q

Which parts of the limbic system are involved in explicit memory

A

Episodic = hippocampus and midbrain

Semantic = frontal temporal lobe

144
Q

Which parts of the limbic system are involved in implicit memory

A

Skills/habits - cerebellum and basal ganglia

Conditioned reflexes - cerebellum and others

Emotional - amygdala

145
Q

What does the amygdala produce and what is it responsible for?

A

Produces instinctive emotional output

Responsible for EMOTIONAL MEMORY and FEAR

PHASE ONE (19 decks)

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