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PTH9111 > Lecture 5- Neural Transmission > Flashcards

Lecture 5- Neural Transmission Flashcards

1
Q

How do neurons communicate

A

Synapses

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2
Q

How do neurons communicate?

A

Firing of action potentials between presynaptic and postsynaptic neurons

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3
Q

Resting membrane potential of an action potential

A

-70mV

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4
Q

Threshold potential of an action potential

A

-55mV

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5
Q

Depolarization

A

When sodium channels open (influx of sodium into axon)

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6
Q

Repolarization

A

Sodium channels close, potassium channels open and potassium moves out

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7
Q

Hyperpolarization

A

Slow closing of K+ channels, Na+ pump establishes resting membrane potential

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8
Q

2 types of synaptic transmission

A
  1. Electrical
  2. Chemical
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9
Q

6 characteristics of electrical transmission

A
  1. Less common
  2. Faster transmission
  3. Pre and postsynaptic cells close together
  4. Protein channels form a physical link at gap junction
  5. Less adaptable (cannot switch form excitatory to inhibitory transmission)
  6. Crucial for formation of neural circuits
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10
Q

7 steps that occur in chemical transmission

A
  1. Action potential activates voltage gated calcium channels
  2. Influx of calcium causes vesicles to fuse with axon terminal membrane
  3. Neurotransmitters released into cleft
  4. Neurotransmitters bind to ligand gated channels on post synaptic cell
  5. Effects are excitatory or inhibitory
  6. Neurotransmitters are destroyed or recycled
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11
Q

Ionotropic Receptor

A

Linked to ion channels and causes immediate effects on post-synaptic potential

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11
Q

2 types of post-synaptic receptors

A
  1. Ionotropic
  2. Metabotropic
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12
Q

Metabotropic Receptor

A

Affects ion channels through intermediates by using G-protein receptors and multiple proteins to produce a slow response

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13
Q

2 types of effects on post-synaptic cells

A
  1. EPSP
  2. IPSP
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14
Q

EPSP

A

Neurotransmitter binding has a depolarizing effect that bring membrane potential closer to threshold to liekly fire an action potential

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15
Q

IPSP

A

Neurotransmitter binding has hyperpolarizing effect and brings potential further away from threshold resulting in no action potential

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16
Q

T or F: IPSPs can be summed with other IPSPs and cannot cancel out EPSP’s

A

False, they can cancel out EPSPs

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17
Q

Spatial Summation

A

Integration of post-synaptic potentials that occur in different locations

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18
Q

Temporal Summation

A

Integration of post-synaptic potentials that occur in same place but different times

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19
Q

Neurotransmitter

A

Signaling molecule that affects another cell (neuron, gland or muscle) across a synapse

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20
Q

Where are neurotransmitters stored and released

A

Stored in synaptic vesicles and released into the synaptic cleft

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21
Q

4 characteristics of glutamate

A
  1. Found in fast excitatory synapses in brain and spinal cord
  2. Major role in synaptic plasticity and memory storage
  3. Binds to ionotropic and metabotropic receptors
  4. Excessive glutamate release can overstimulate cells and is neurotoxic
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22
Q

What 4 disorders can excessive glutamate cause

A
  1. Ischemic stroke
  2. Epilesy
  3. Alzheimers Disease
  4. Parkinsons Disease
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23
Q

2 facts about GABA

A
  1. Fast inhibitory synapses in brain
  2. Sedatives/substance abuse enhance effects of GABA
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24
Q

Pyridoxine Deficiency

A

Vitamin B6 is not available for synthesis of GABA leading to frequent seizures

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25
Q

T or F: Dystonia and spasticity are related to deficiencies in dopamine signaling

A

F, GABA signaling

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26
Q

What neurotransmitter partially causes Huntington’s disease and why?

A

Lack of Gaba in striatal projections in the globus pallidus

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27
Q

T or F: The brain has a single dopamine pathway

A

F, it has several pathways

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28
Q

Dopamine has a major role in

A

Reward-motivated behavior’s

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29
Q

Anticipation of reward [increases/decreases] dopamine level in the brain

A

Increases

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30
Q

T or F: Addictive substances increase dopamine release or block its reuptake

A

T

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31
Q

Parkinson’s disease is caused by what and why

A

Loss of dopamine secreting neurons in the substantia nigra

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32
Q

What is a treatment for Parkinson’s disease

A

Levodopa (L-DOPA)

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33
Q

What neurotransmitters altered levels triggers schizophrenia

A

Dopamine

34
Q

What drugs are used to treat schizophrenia

A

Antipsychotic drugs (dopamine antagonists = reduce dopamine levels)

35
Q

Norepinephrine 7 functions

A

Mobilize brain and body for action by:
1) influencing sleep/wakefulness
2. Attention
3. Memory formation/retrieval
4. Increased restlessness
6. Anxiety
7. Stimulates release of epinephrine (stress hormone)

36
Q

What is the major peripheral neurotransmitter used by sympathetic nervous system to increase heart rate, blood pressure, and blood flow to skeletal muscles during fight or flight?

A

Norepinephrine

37
Q

Noradrenaline

A

Injectable drug that lowers blood pressure

38
Q

Alpha and beta blockers

A

Block effects of adrenergic receptors

39
Q

When would you use alpha and beta blockers

A
  1. Cardiovascular disease (lowers BP)
  2. Anxiety disorder
  3. Panic Disorder
40
Q

Where is Serotonin mainly produced

A

Gastrointestinal Tract (90%)
**1-2% in CNS

41
Q

Serotonin 5 functions

A

Regulates mood, behavior’s, appetite, temperature, and sleep

42
Q

Acetylcholine’s 4 roles in the brain

A
  1. Arousal
  2. Attention
  3. Memory
  4. Motivation
43
Q

Acetylcholine’s 2 roles in the Parasympathetic Nervous System (PNS)

A

Vasodilation and blood flow to organs in the rest and digest response

44
Q

What is acetylcholine’s role in skeletal muscles

A

It is a neurotransmitter at the neuromuscular junction that connects motor nerves to muscles. It activates skeletal muscle involuntary movements

45
Q

How does venoms, toxins and chemical nerve agents influence acetylcholine at the neuromuscular junction

A
  1. Prevents breakdown of acetylcholine at the junction
  2. Acetylcholine builds up triggering constant action potentials and muscle contractions
  3. Paralysis and then death
46
Q

Myasthenia Gravis

A

Long-term neuromuscular junction disease that blocks or destroy acetylcholine receptors preventing action potentials from triggering muscle contractions. Causing skeletal muscle weakness around the eyes, face, swallowing, and potentially respiratory muscles.

47
Q

How to treat myasthenia gravis

A

Acetylcholinesterase inhibitors and immunosuppressants

48
Q

What is substance P

A

A neuropeptide that is a first responder to noxious or extreme stimuli that may compromise bodily integrity (immediate stress, defense, repair, and survival system)

49
Q

Where is Substance P synthesized

A

Dorsal root ganglia (present in nerve endings in primary afferents such as skin, muscle, and joints)

50
Q

What are 2 ways that substance P mediates inflammation and tissue repair?

A
  1. Potent vasodilation
  2. Initiates expression of cytokines
51
Q

Classification System 1 (Nerves)

A

Based on conduction velocity of different types of motor and sensory nerve fibers

52
Q

Conduction speed of a nerve is based on what 3 factors

A
  1. Myelination
  2. Nerve Length
  3. Nerve Diameter
53
Q

Classification System 2 (Nerves)

A

Numerical classification of sensory nerve fibers

54
Q

How do we measure action potentials in muscles?

A

Needle electromyography (EMG)

55
Q

Action potentials appear when a muscle is [voluntarily/involuntarily] contracted

A

Voluntarily

56
Q

T or F: As contraction strength increases, less action potentials appear

A

F, as contraction strength increase more action potentials appear

57
Q

When do we usually perform an EMG

A

Alongside a nerve conduction study

58
Q

What 3 things does a nerve study establish?

A
  1. If motor/sensory nerve cell bodies or peripheral nerves are damaged
  2. If the primary target is the axon or myelin sheath
  3. If the nerve damage is generalized (higher up and affects a lot of nerves), multifocal (affects few nerves), focal (affects 1 nerve)
59
Q

Neurapraxia

A

Mildest form of traumatic peripheral nerve injury that causes focal segmental demyelination at site of injury resulting in nerve conduction and transient weakness (paresthesia). Able to completely recover with spontaneous myelination.

60
Q

Axonotmesis

A

Axon and sheath damaged but connective tissue intact that requires regrowth of axon to target muscle, but can be impeded by scar tissue formation

61
Q

Neurotmesis

A

Complete rupture of nerve with no chance of recovery. Surgery is required.

62
Q

Peripheral neuropathies

A

Damage/disease affecting peripheral nerves that causes sensations of numbness, weakness, tingling or pain (pins & needles/burning)

63
Q

What is the most common cause and some other causes of peripheral neuropathies

A

Most Common: Diabetes
Others: Trauma, medication (antibiotics or chemotherapy), celiac disease, immune system disease, and viruses

64
Q

Mononeuropathy

A

Affects a single nerve

65
Q

Polyneuropathy

A

Affects multiple nerves

66
Q

Demyelinating Disease

A

Damage or disease to myelin sheath surrounding nerves causing action potentials to slow or stop

67
Q

2 ways for demyelinating diseases to form

A
  1. Healthy myelin destroyed by toxic substances, chemicals, or autoimmune reactions
  2. Myelin is abnormal and degrades over time
68
Q

Name 2 diseases that are demyelinating diseases and describe them

A
  1. Multiple Sclerosis: Destruction of myelin by immune system of neurons in brain and spinal cord
  2. Guillain-Barre Syndrome: Rapid onset of muscle weakness caused by immune system attacking peripheral nervous system
69
Q

Muscle Atrophy

A

Loss of skeletal muscle mass (denervation of muscle results in death of muscle fibers because of imbalance between protein synthesis and degradation) causing damage to central and peripheral nerves

70
Q

4 ways to delay, prevent or reverse muscle atrophy

A
  1. Exercise
  2. Electrical stimulation (when paralysis is present)
  3. Adequate calorie and protein intake
  4. Anabolic steroids
71
Q

Critical Illness Polyneuropathy

A

Diffuse, symmetrical muscle weakness in critically ill patients involving all extremities and diaphragm.

72
Q

What are 2 side effects of critical illness polyneuropathy

A
  1. Respiratory difficulties b/c atrophy of diaphragm and intercostal muscles (degeneration of phrenic nerve)
  2. Prolonged time to wean someone off mechanical ventilation
73
Q

3 ways to reduce symptom severity of critical illness polyneuropathy

A
  1. Mobility
  2. Passive Stretching
  3. Electrical Stimulation
74
Q

Synaptic Plasticity

A

Biological basis for learning, memory and recovery of function after illness or injury

75
Q

4 mechanisms of synaptic plasticity

A
  1. Change synaptic strength
  2. Synaptic Elimination
  3. Synaptogenesis
  4. Neurogenesis
76
Q

T or F: Synaptic strength is shaped by experience (cognitive, physical, social and emotional)

A

T

77
Q

3 ways to increase synaptic strength in the presynaptic cell

A
  1. Increase size of presynaptic terminal
  2. Increase number of axons
  3. Increase quantity of neurotransmitter
78
Q

3 ways to increase synaptic plasticity of postsynaptic cell

A
  1. Growth of dendritic spines
  2. Increase receptor zone
  3. Increase number of receptors
79
Q

T or F: Physiotherapists should drive beneficial changes in synaptic strength to minimize or reverse maladaptive changes in synaptic strength in individual who had strokes, are critically ill, or suffer from chronic pain

A

T

80
Q

Explain how a stroke affects the hemisphere

A

Lesioned hemisphere exerts less inhibition over non-lesioned hemisphere, allowing the non-lesioned hemisphere to take over, reducing the ability of the lesioned hemisphere to recover through synaptic plasticity

81
Q

Explain transcranial magnetic simulation (TMS) treatment in stroke patients

A

put it over head and put high frequency pulses into brain to increase excitability in lesioned hemisphere of stroke victims, and reduce amount of control in non-lesioned hemisphere = balance hemispheres to give lesioned hemisphere better chance of increased plasticity

82
Q

How is synaptic plasticity linked to chronic low back pain

A

Increased plasticity occurs when pain reoccurs continuously that it eventually builds permanent connections. This results in people experiencing chronic back pain instead of just acute back pain. (Short/Long multifidus fibers diagram shows that in people who experience chronic pain, both fibers are activated immediately due to greater synaptic plasticity in comparison to those who don’t experience pain)

83
Q

What is one possible way to potentially treat chronic pain (low back pain)

A

Use electrical stimulus on both the area of pain and brain to try and revert synaptic plasticity to atypical levels to reduce chronic back pain

PTH9111 (15 decks)

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