Module 3 - Nervous System Flashcards

Nervous system

1
Q

Neuron count of CNS

A

100 billion in brain, 13.5 million in spinal cord

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2
Q

How many glial cells (supporting cells in CNS) do we have?

A

10^11

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3
Q

How many genes participate in the formation of the nervous system?

A

40%

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4
Q

What is the basic building block of the nervous system?

A

The neuron

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5
Q

2 subdivisions of the nervous system

A
  1. CNS
  2. PNS
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6
Q

2 gross subdivisions of CNS

A
  1. Brain (encephalon)
  2. Spinal cord
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7
Q

5 Anatomical divisions of CNS

A
  1. Cerebrum
  2. Diencephalon (thalamus, hypothalamus, epithalamus)
  3. Brain stem
  4. Cerebellum
  5. Spinal cord
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8
Q

Parts of the brain stem

A

Top part of brain stem: Midbrain
Middle part: Pons
Bottom: Medulla oblongata

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9
Q

Roles of the different roots of spinal cord

A

Dorsal root of spinal cord is sensory
Ventral root of spinal cord is motor

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10
Q

How does the brain receive information

A

From receptor, sensory nerve carries signal via dorsal root. The brain will then send information out the ventral root through efferent neurons through motor neurons to effectors.

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11
Q

Dorsal root ganglion has connections with?

A

ANS to ensure that reactions occur e.g. painful stimulants.
This is located on the dorsal root

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12
Q

2 parts of PNS

A
  1. Autonomic Nervous System - involuntary movements
  2. Somatic Nervous System - voluntary movements
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13
Q

ANS is divided into 3 parts…

A

Parasympathetic - rest and digest
Sympathetic - Systems become activated
Enteric - In GI, makes sure digestive system works without thinking about it

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14
Q

Purpose of cerebrospinal fluid (CSF)

A

Provides nutrition to the brain since its an ultrafiltrate of blood plasma (allows certain things to be included in e.g. allowing a lot of glucose in cerebrospinal fluid due to high energy requirements.)

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15
Q

Quantity of CSF

A

150mL

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16
Q

Where is CSF produced and is lined by?

A

Ventricles of the brain and are lined by specialised cells called choroid plexus (network)

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17
Q

What happens if there is not enough CSF

A

It is going to accelerate neurodegenerative diseases (e.g. Parkinson’s, Alzheimer’s).

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18
Q

What happens if there is too much CSF

A

Head swells up and pushes eyeballs down: Setting sun sign

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19
Q

Grey matter vs white matter

A

Grey matter sits towards peripheral or circumference of brain. High nucleus count due to high neuron count.

White matter - because axons in the brain are covered in myelin, white matter is closest to the central region of brain. This high myelin count causes the colour to become white.

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20
Q

What happens to the grey and white matter in the spinal cord?

A

It reverses - white matter on outside and grey matter on inside

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21
Q

Wernicke’s aphasia

A

Cannot comprehend language but can speak properly so speech becomes voluble - doesn’t make sense.

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21
Q

Function of occipital lobe

A

Vision

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21
Q

Function of frontal lobe

A

Motor control, personality, problem solving, speech production (Broca’s area)

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22
Q

Function of parietal lobe

A

Sensory

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23
Q

Function of temporal lobe

A

Auditory processing, language comprehension, Wernicke’s area, memory/information retrieval

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24
Q

Broca’s aphasia

A

They are able to think and understand language but cannot articulate their words.

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24
Q

What do macroglia do?

A

Provide structural support to nervous system

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24
Q

Function of cerebellum

A

Balance and coordination

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25
Q

Function of brain stem

A

Involuntary responses e.g. breathing

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26
Q

Epineurium

A

Outermost layer enclosing nerves

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26
Q

Structure of typical spinal nerve

A

Each of the axons that arise from the nerve cell body is enclosed by connective tissue sheath called endoneurium. Perineurium encloses fascicles. A lot of nerve fascicles come together and enclose in the epineurium - ensures nerves are well protected

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27
Q

What is a bundle of axons called

A

Fascicle

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28
Q

Perineurium

A

Middle layer

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28
Q

What are the 2 macroglia cells called in the PNS

A

Schwann cells and satellite cells.

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29
Q

Role of oligodendrocytes in CNS

A

Produce myelin across multiple axons in CNS

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29
Q

Endoneurium

A

Innermost layer

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30
Q

What are microglia

A

Are like scavengers: clear dead debris and dead neurons through phagocytosis.

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30
Q

2 general types of cellular elements in the CNS

A
  1. Microglia
  2. Macroglia
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31
Q

Role of ependymal cells

A

Help generate CSF

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31
Q

What are the 3 macroglia in the CNS called?

A

Oligodendrocytes, astrocytes, ependymal cells

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31
Q

How to remember the cells involved in macroglia

A

MEAO (pronounced meow).
M: Macroglia
E: Ependymal cells
A: Astrocytes
O: Oligodendrocytes

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32
Q

Role of astrocytes

A

Creating Blood Brain Barrier (BBB)
Ensuring only required things go into CSF e.g. want to leave out large proteins and white blood cells but glucose can go in.

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32
Q

Role of Schwann Cells in PNS

A

Produces myelin in nerves so if peripheral nerve gets cut, Schwann cells can provide conduit for which nerve can grow. This is why the PNS can restore cells but CNS cannot restore brain cell

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33
Q

Before an axon is myelinated, there is…

A

An initial segment of axon and is then covered in myelin sheaths which then activates buttons that activate effectors. Nodes of Ranvier are not covered by myelin sheath.

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34
Q

2 types of axonal transport

A
  1. Axonal orthograde (anterograde) transport
  2. Retrograde transport
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35
Q

What is axonal orthograde transport and what does it utilise

A

When material that a nerve cell body has prepared, it goes from the cell body to axon terminal buttons. e.g. neurofilaments, synaptic vesicles

They utilise microtubules made of tubulin

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36
Q

Specific protein used in anterograde transport

A

Kinesin

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37
Q

What is retrograde transport?

A

Moving back to nerve cell body e.g. endosomes, injury signals.

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38
Q

Protein used in retrograde transport

A

Dynein

39
Q

What needs to happen for us to change RMP

A

needs to have concentration gradient - will determine whether a cell fires or not.

40
Q

What needs to happen to ensure the RMP can change

A

We need channels on the cell membrane: Ligand-gated channels (opens when a ligand e.g. neurotransmitter binds to them) or voltage-gated ion channels (has to be a change in potential difference to open)

41
Q

7 steps of Action Potential

A
  1. Changes in membrane conductance of Na+ and K+: when Na+ sodium channels open, RMP becomes more positive (-70 to become around -55 - threshold potential) due to rush of Na+ into the cell
  2. Positive feedback loop: Entry of Na+ causes the opening of more voltage gated Na+ channels so more and more Na+ enters the cell
  3. Na+ causes membrane potential to move towards the equilibrium potential for Na+ (60mV) but does not reach it during AP. The Na+ channels rapidly close and enter inactived state and remain in this state for a few milliseconds before returning to the resting state when they again can be activated.
  4. K+ channels open, causing repolarisation - decreasing RMP voltage. K+ channels will stay open until threshold potential is reached (–55mV)
  5. Opening of more voltage gated K+ channels is slower and more prolonged than the opening of Na+ channels
  6. Net movement of positive charge out of cell due to K+ efflux helps complete repolarisation. The slow return of K+ channels to the closed state explains after-hyperpolarisation
  7. Return to RMP. Thus, voltage gated K+ channels bring AP to an end and cause closure of their gates through negative feedback process.
42
Q

What is the direction of electrical gradient during the overshoot (peak voltage in AP)

A

It is reversed because the membrane potential is reversed which limits Na+ influx.

43
Q

What happens when the membrane potential hits 30mV?

A

Na+ channels close and K+ stays open. This is when we utilise Na+/K+ pumps: For every 3 Na+ out, 2 K+ comes in.

44
Q

Why do we need to get rid of sodium inside the cell?

A

Because if it stays inside the cell, it will attract a lot of water, making processes harder and slower

45
Q

When membrane is undergoing repolarisation, it is unable to become…

A

Excited when it is an absolute refractory period. Can only be excited in relative refractory period.

46
Q

Repolarisation =

A

K+ influx, Na+ efflux.

47
Q

All or none law

A

States that once a threshold stimulus is reached, a neuron or muscle fibre will fire an AP in its entirety or not at all

48
Q

3 key points of the All or none law

A
  1. Threshold stimulus: For a neuron or muscle fibre to fire, the stimulus must be strong enough to reach certain threshold e.g. You will feel a hand on your shoulder but may not feel a feather
  2. Action potential: once threshold is reached, AP is generated and propagated along the entire length of the neuron or muscle fibre without diminishing in strength (i.e. amplitude of AP needs to be enough to propagate through entire nerve) People who have MS where myelin sheath is damaged, info is lost hence causing problems like breathing
  3. Binary response: The response is “all” if the stimulus reaches the threshold, meaning full AP occurs. It is “none” if the stimulus does not reach the threshold meaning no AP occurs.
49
Q

Electrotonic potentials

A

AP that is of low amplitude

50
Q

Role of excitatory postsynaptic potential (EPSP)

A

Will excite neuron to threshold value so that it can fire.
Makes membrane less negative

51
Q

Another name for EPSP

A

Depolarising potential since they have potential to have AP to occur.

52
Q

Where is EPSP usually?

A

In post-synaptic cell which becomes more positive so more sodium flux

53
Q

What does EPSP result from?

A

Influx of Na ions into post-synaptic neuron. You also need a neurotransmitter to get to the postsynaptic neuron

54
Q

Common excitatory neurotransmitters involved in EPSP

A

Glutamate and acetylcholine

55
Q

When EPSP occurs, there’s a likelihood its..

A

Just 1 - causing twitch or multiple (able to lift weight in gym)

56
Q

Role of Inhibitory Postsynaptic Potentials (IPSP)

A

Makes membrane more negative by inhibiting certain functions e.g. spasms

Ensures we do not activate our muscles a lot and closer to the resting state than excited state

Decreases likelihood that post-synaptic neuron will reach threshold potential: can filter out signals that are not needed e.g. in Chorea, people fling their arms in a random way since their inhibitory signals are lost so they’re unable to control it.

57
Q

What causes IPSP

A

Flux of Cl- and efflux of K+: keeps membrane more negative

58
Q

Neurotransmitters involved with IPSP

A

Gamma-Aminobutyric Acid (GABA) and Glycine

59
Q

2 ways a membrane can be excited

A
  1. Temporal summation: one neuron, one effector
  2. Spatial Summation: More than 1 neuron connected to other neurons. Has to differentiate which neuron is excitatory and inhibitory
60
Q

How do Local Anaesthetics (Lognocaine) work?

A

Reversibility inhibits nerve transmission by binding voltage gated sodium channels in the nerve plasma membrane. In other words, they block the entry of sodium into the cell. So, if sodium is blocked, AP does not occur thereby preventing pain

61
Q

2 types of conduction

A

1.Orthodromic
2. Antidromic

62
Q

Orthodromic conduction

A

Propagation of AP in natural forward potential from soma down the axon to axon terminal. Ensures signals are transmitted from presynaptic neuron to postsynaptic. `

63
Q

Antidromic conduction

A

propagation of AP in reverse direction from axon terminals back towards the soma.
can be used to identify neuron by stimulating axon terminal and observing the retrograde AP reaching the soma - this is how we manipulate and tell the nerve that it has reached its destination and doesn’t need to fire anymore

64
Q

Biphasic action potentials:

A

Determining whether electrodes can register positive or negative voltage

65
Q

3 types of nerve fibres

A

A, B and C fibres

66
Q

Characteristics of A fibre

A

Myelinating (conducts really fast) e.g. outside in cold and feeling cold win instantly.
Carries somatic motor
Function is also touch and pressure, pain, temperature
In diabetes, where touch is impaired, A fibres are deficient.

67
Q

Characteristics of B fibres:
Associated with…
These fibres sit between

A

Preganglionic autonomic
Associated with ANS.
Before autonomic fibres synapses with ganglion, fibres that sit between ganglion and spinal cord are B fibres
Associated with visceral function (lungs, stomach, heart)

68
Q

Characteristics of C fibres:

A

Un-myelinated
Functions of pain and temperature too but where it is slower than A fibre e.g. when shower is hot and eventually feels cold. Because they are so slow, they are only good for carrying information from visceral regions.

69
Q

Nerve fibres are very vulnerable to?

A

Oxygen saturation - the moment you reduce O2 oxygen saturation, nerve fibres start to die. This is why there’s a 5 minute window after someone collapses and heart and lung stops functioning. If you cannot bring them back before 5 minutes, you die or get brain damage

70
Q

Neurotrophins

A

Protein needed for neurons to survive and function:
In Alzheimer’s there’s plaques in the brain so we are unable to get neurotrophins to site of injury. So, nerves are not repaired or generated.

71
Q

Principal sensory modalities:

A

Touch
Proprioception

72
Q

What is proprioception?

A

Located in joints and tendons. E.g. tells foot where its going to go when foot is going on the floor

73
Q

How does the nervous system encode and interpret strength or intesntiy of stimulus

A

When we are touched, sensory units are recruited. This determines whether its a pat on the back or feather on shoulder

74
Q

2 types of potentials:

A
  1. Generator
  2. Receptor
75
Q

Where are generator potentials mainly seen?

A

Receptors

76
Q

Where are receptor potentials mainly seen

A

In receptors that carry information of different intensity (touching shoulder vs touching with feather)

77
Q

3 laws of specific nerve energies and projection:

A
  1. Specificity of nerves (each nerve is dedicated to a certain function)
  2. Perception of stimuli: depends on receptor density e.g. if receptors are concentrated in a certain area, they will be very sensitive e.g. fingers and lips are sensitive vs the back not as sensitive otherwise clothes become uncomfortable
  3. Implications: Excitatory and postsynaptic potentials depend on the type of stimulus: excitatory or inhibitory
78
Q

Why does phantom limb occur

A

Because of the nerve sensitivity, the nerve that goes to the foot will always think its going to the foot (as per law 1 of the nerve energies and projection)

79
Q

Axodendritic:

A

1 neuron synapses with dendrites of another

80
Q

Axosomatic:

A

Axon of a neuron synapses with cell body of another

81
Q

Axoaxonic

A

Axon of neuron synapses with axon of another neuron

82
Q

What are the organelles responsible for generating vesicles within the nerve?

A

Endosomes

83
Q

6 processes of synapsing

A
  1. Vesicles bud off endosome.
  2. Vesicles fill up with neurotransmitter
  3. It is translocated (moving towards active site on synapse)
  4. It is then docked (requires ATP) - ensures vesicle is ready to undergo exocytosis - putting its contents into synaptic cleft.
  5. This can’t occur until there’s Ca flux
  6. Once neurotransmitter is released and AP has passed, vesicle is taken back into endosome through endocytosis and translocation
84
Q

Important proteins in synaptic vesicle docking and fusion

A

SNAP and SNARE.
With the role of ATP and Ca, they reel the vesicle into neuron

85
Q

Reflex arc

A

Receptor from sense organ travels through afferent (sensory) neuron. Will carry information to CNS (Spinal cord). Then a motor nerve (efferent neuron) carries information to muscle (effector)

86
Q

Bell Magendie Law

A

Sensory cannot carry motor information and motor cannot carry sensory information.
They can only travel in 1 direction - cant define their own direction

87
Q

Reflexes can be…

A

Monosynaptic - 1 synapse
Polysynaptic: Multiple Synapses

88
Q

What specialised receptors in musculoskeletal system makes sure muscles contract properly and operate muscle tone

A

Muscle spindles - are stretched whenever muscles are stretched.

89
Q

Reciprocal innervation

A

At any time, agonists contract, opposing group (antagonist) must relax.

90
Q

Inverse stretch reflex

A

Have reached limit of maximum contraction and now you have to start relaxing. We want to make sure that if they are contracting, they need the ability to relax.

91
Q

Muscle tone

A

Continuous and passive partial contraction of muscles or the muscles resistance to passive stretch during resting state

92
Q

What test tests monosynaptic reflex

A

Knee jerk - Minute change in patellar tendon is enough to stretch muscle spindle which causes sensory neuron to go to posterior spinal cord. It then synapses with a neuron that is anterior which causes motor neuron to come out and move the muscle.

93
Q

Process of a polysynaptic reflex

A

Fibres that carry information to dorsal grey matter of spinal cord, they synapse with an extra neuron (interneuron - within grey matter). These neurons then communicate with efferent fibre out of the ventral grey matter of spinal cord. 1 neuron activates muscle and then another neuron relaxes the antagonist (reciprocal innervation)

94
Q

What is the withdrawal reflex?

A

A polysynaptic reflex that protects the body from harmful stimuli e.g. to withdraw arm from flame, need bicep to move and tricep to relax.

95
Q

2 concepts associated with withdrawal reflex

A
  1. Fractionation: activating particular group or type of nerve depending on the stimulus
  2. Occlusion: has to choose stimulus that is beneficial to an organism e.g. thirst and hunger isn’t a priority but withdrawing finger from flame is.
96
Q

Crossed extensor reflex

A

Polysynaptic reflex. Helps maintain balance by coordinating the opposite limbs response e.g. on beach, stepping on shell. Affected leg withdraws and other leg tightens up so you dont fall.

96
Q

Neuromuscular junction steps:

A
  1. Motor neuron AP generated (travels in antegrade direction - from nerve cell body to synapse): orthodromic conduction
  2. Ca2+ entry voltage gated channels are activated on presynaptic membrane
  3. Acetylcholine is released via exocytosis which then activates:
  4. Ligand gated Na+ channels on postsynaptic membrane
  5. Local current between depolarised endplate and adjacent muscle plasma membrane
  6. Muscle fibre AP initiation
  7. Propagates AP in muscle plasma membrane
97
Q

After acetylcholine is used, what breaks it down?

A

Acetylcholinesterase breaks acetylcholine into 2 parts to re-generate acetylcholine until AP ceases.

98
Q

If an axon degenerates…

A

Becomes more sensitive to acetylcholine. This causes denervation (loss of nerve supply) which then leads to upregulation of acetylcholine receptors.

98
Q

Neuromodulators

A

Chemicals released by neurons that may modify the effects of neurotransmitters.

99
Q

What does the presynaptic receptor (autoreceptor) often inhibit, providing feedback control?

A

Inhibits further release of neurotransmitters. Comes from proximal receptor (near neck_ and goes to distal receptor and will produce a negative feedback that lets the body know that no more neurotransmitters are needed

99
Q

Presynaptic heteroreceptor

A

Same mechanism as autoreceptor but instead of adrenaline acting on receptors, it acts on cholinergic nerve terminals

99
Q

Receptors are grouped into 2 large families based on structure and function

A
  1. Ligand-Gated Channels (Ionotropic receptors) - when activated, flux of ions
  2. Metabotropic receptors (G-protein coupled receptors): Associated with metabolic pathways e.g steroid hormones. REQUIRES ATP
99
Q

Process of neurotransmitter reuptake

A

Release of neurotransmitter to generate impulse (AP) then binds to receptors and brings about changes in the membrane. Gets broken down and repackaged into synaptic vesicle for future release.

100
Q

3 different things we can do to neurotransmitters once its role has been fulfilled

A
  1. Digest the signal so the signal gets terminated e.g. if we want to remove inhibitory signal so we can excite muscle
  2. Recycle it
  3. Regulate synaptic activity via reuptake
101
Q

How does the use of SSRI’s work?

A

Under normal circumstances, serotonin will be broken down and put back into the cell for the new impulse. However, SSRI’s inhibit the reuptake of serotonin, meaning it is available in the neurons for longer

102
Q

Effect of increased temperature on a nerve

A
  1. Increased energy available via heat on the outside. Temperature must not rise (must stay at 37c) which means nerves start to fire more rapidly due to homeostasis to try and get more information to have homeostatic mechanisms in place. More AP are propagated and generated (shortens impulse-duration: more AP, higher frequency)
  2. Metabolic rate goes up which means more enzymes break down molecules and convert it to energy. When temp increases, the cell membrane stretches which means the ion membranes will increase in diameter, predisposing them to taking in more ions.
  3. Reduced threshold for activation: warmer temps lower threshold for AP initiation, making neurons more excitable
  4. Potential for hyperexcitability
103
Q

Effect of decreased temperature on nerves

A
  1. Slower conduction velocity
  2. Increased threshold for activation
  3. Potential for conduction block: AP fails to propagate leading to conduction block causing numbness or loss of function
  4. Impaired enzyme activity (ion pump functions and metabolism reduces at lower temps which can impair nerve function)
104
Q

Why is temperature only proportional to nerve conduction velocity to a certain point?

A

Our cells have a finite capacity of nutrients for an AP to occur. Once you reach that capacity, it will take a while to replenish.

105
Q

Warming of nerves reduces the… because…

A

Reduces the peak amplitude because the shorter duration of Na current reduces its ability to charge the membrane close to Ena.