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KIN 3E03 > Test 2 > Flashcards

Test 2 Flashcards

1
Q

Glia

A

-Greek for glue
-Insulate, support and noursih neurons
-may even influence processing
-coookie portion of chocolate chip cookie

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2
Q

neurons

A

-Processes information
-Sense information
-Sense envrionemental changes
-Communicate changes to other neurons
-Command body response
-Chocolate chips of chocolate chip cookie

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3
Q

soma

A

-Greek for body
-AKA- cell body or perikaryon
-contains nucleus and many organelles

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4
Q

neurites

A

-anything coming off soma includes:
dendrites- receive info
axons- send info

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5
Q

nerve vs neuron

A

neruon: cells that sends and receives electrical signals
nerve: a group of fibers (axons) that carry information

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6
Q

The soma: cytosol

A

-watery fluid inside the cell, seperted from outside by neuronal membrane

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7
Q

The soma: Organelles

A

-membrane enclosed structures within the soma
-nucelus, endoplasmic reticulum, mitochondria

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8
Q

The soma: Cytoplasm

A

-Everything contained within the cell membrane
Cytoplasm= cytosol + organelles - nucleus

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9
Q

Neuronal membrane

A

-Barrier that encokeses cytoplasm and regulates membrane potential
-embeded within proteins that grant aess and regulate concentrations
-structure of membrane varies based on neuron regions

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10
Q

cytoskeleton of neuron

A

-“bones” of the neuron (providing rigidity)
-Not static- continually remodelling and in motion
-Three structures: microfilaments, neurofilaments, microtubules

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11
Q

infographic

A

a way to communicate important informaiton in a more engaging way

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12
Q

What causes Alzheimer’s disease

A

dominant theory has been build of plaque
-Amyloid hypothesis- plaque build uo on neuorns. Proteins not being cleared- build uo causes plaque that impacts brain communication
Although this is the dominant theory, plaque busting drugs have yet to show a lot of clincally significant improvements to symptoms

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13
Q

controversy of alzeimers drugs

A

speed of approval, yet to see lots of actual symtomatic imprvments. Drugs do in fact break down plaque- but seeing that it doesnt necesarly help QOL or symptoms
now seeing that some publications are making nots on early data

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14
Q

What else may be cuaseing alzheimers disease

A

Structure of axon is another major theroy
-Tau hypothesis
tangling of microtubiles may precede plawue formation
-variety of clinical trials with limited success

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15
Q

Tau and amyloid hypothesis together

A

likely these is a synergistic dance between amyloid and tau
-both occur together in patients with alzheimers disease
-inflammation and vasular dysfunction may initiate of accelerate the process

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16
Q

Axon length

A

Can range from less than 1mm to over 1m
not always a direct path- axon collaterals

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17
Q

Three areas of an axon

A

axon hillock (beginning)
axon proper (middle)
axon terminal (end)
note- synapse is the point of contact

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18
Q

axon thickness

A

humans- 1-25 nanometers in diameter
-generally, the thicker the axons, the faster the signal travels

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19
Q

How is the axon terminal different from the rest of the axon

A

-no microtubules in terminal
-has synaptic vesicles
-abundance of membrane proteins
-large number of mitochondria

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20
Q

axon synapse

A

-provides the contact site for transmission of signal (eg. electric-chemical-electric)
-Presynaptic (sends signal) vs postsynaptic (receives signal)

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21
Q

Dendrites

A

Greek for tree
-dentritic tree (all) with dentritic branches (individual)
-the “antennae” of neurons and covered in thousands of receptors- -roange dots on immunohistochemistry
-receptors ro receive neurotransmitters

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22
Q

classification of neurons based on number of neurites

A

-single neurite (unipolar)- sensory nerve with dorsal root gangilon
-two neurites (bipolar)- vestibulocochlear
-more than 2 neurites (multipolar)- many neurons in the body

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23
Q

classification of neurons based on dendritic and somatic morphology

A

-satate cells (star shaped)
-pyramidal cells (pyramid-shaped)

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24
Q

classification of neurons based on connections woth the cns

A

-primary sensory neruons
-motor neurons
-interneurons

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25
Q

classification of neurons based on axonal length

A

-golgi type I- long; go to other areas
-golgi type II- short; remain local

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26
Q

2 primary tpes of glia

A

astrocytes and myelinating glia

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27
Q

astrocytes

A

-most numerous glia in the brain
-fill spaces between neurons
-influence whether neurite grow/retract
-regulate chemical contect of extracellular space

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28
Q

myelinating glia

A

-insulate to faciliate transmission
-oligodendroglia (in CNS)
Canprovide myelin for multiple axons
-Schwann cells (in PNS)
Only provide myeling for one axon

Node of ranvier- region where axonal membrane is exposed

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29
Q

neural communication- electrical signal transmission by region

A

dendrites: initiate signal and pass towards axon
Axon hillock: action potential (AP) begins
Axon (axon proper): AP travels toawrds terminal
Axon terminal: receives AP and sends to other cells
Electrical signal is the change in electrical potential of the neuron (change in resting membrane potential)

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30
Q

Resting membrane potential

A

-difference between the inside (cytosol) and outside (extracellular membrane potential)
-typically -70mV
-Based on concentrations of NA+, K+, and Cl-

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31
Q

Membrane states: polarization

A

state wehn membrane potential is other than 0mV
(move away from zero)

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32
Q

Membrane states: depolarization

A

membrane becomes less polarized than at rest (moves to 0)

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33
Q

Membrane states: hyperpolarization

A

membrane becomes more polarized than at rest (even further away from zero)

34
Q

Membrane states: repolarization

A

membrane returns to resting potential after a depolarization (away from zero)

35
Q

2 kinds of membrane potential changes

A

graded potentials and action potentials

36
Q

graded potentials

A

-serves as short distance signals
-initiated at dendrites (electrically, chemically, or mechincally) and passed towards axon (hillox)

37
Q

action potentials

A

-serve as long-distance signals
-start at axon hillock quickly passed to axon termals

38
Q

Properties of graded potentials (4)

A
  1. local (die quickly)
  2. summation- no refractpry period
  3. can vary in intensity
  4. can be excitatory-EPSP (depolarizing) or inhibitaroy-IPSP (hyperpolarizing)
39
Q

summation (2 types)

A

spatial summation: generated simultaneously at different sites
temporal summation: generated at same site in rapid succession
no refractory period

40
Q

graded potential to action potential

A

action potential occurs at the spike initation zone if graded potentials break threashold (-55mV)

41
Q

States of the action potnetial

A

1.sufficient stimulus to break threashold
2. Rising phase: rapid depolarization (NA+ in)
3.Falling phase: membrane repolarization (K+ out)
4. Hyperpolarization below resting potential
-absolute refractory period (no stacking- unlike graded potentials)
-relative refractory period (due to hyperpolarized state)
5. resting membrane potential returns

42
Q

key properties of the action potential

A
  1. all or none
    -either produce an AP or not (singals are binary: on vs off, -1 vs 0)
  2. firing rate conveys important information
    -must code information in timing rather than magnitude of singal
43
Q

Factors influencing conduction velocity

A

axon diameter
-bigger axons are faster- reduced resistance to flow
-survival pathways generally larger
myelin layers
-allow AP to jump across the axon (Nodes of ranvier)
-Schwann (PNS) vs Oligodendroglia (CNS)

44
Q

continous conduction

A

-Unmelyinated fibers
– Action potential spreads along every portion of the membrane

45
Q

saltatory conduction

A

-myelinated fibers
-Impulse jumps across breaks in myelin (node of Rnavier)
-~50x faster!

46
Q

Multiple Sclerosis

A

-Autoimmune disorder characterized by the loss of myelin in the CNS (doesn’t impact the PNS)
-Decreased speed of nerve impusles (@regions below damage)

47
Q

Multiple Sclerosis symotoms/ manifestation

A

-decreased speed of nerve impulses
-sensory- numbness, tingling and pain
-motor- loss of coordination in muscles
-Symptoms are highly variable within and between patients

48
Q

Risk factors for MS

A

Age: Most diagnosed between 20-49 years of age
Genetics: Family history greatly greatly increases risk
other factors: infections, race, climate, vitamin d, diet, smoking
living in Canada” ~300 in every 100, 000 canadians

49
Q

MS treatment

A

-No cure
-treat symtoms and progression with a variety of drugs (eg, mixed outcomes/side effects)
-Exercise can improve mobility, fatigue levels, and overall quality of life in MS patients (especially for mild-moderate patients…)

50
Q

Slope walking and MS

A

where less myelin disruption was associated with greater intervention response

51
Q

synapses

A

junctions between two neruons
-means by which one neuron interacts with another neuron
-first neuron: presynaptic neuron
-target cell: postsynaptic neruon

52
Q

arrangements of synapses

A

axodendritic: axon-dendrite
axosomatic: axon to cell body
axoaxonix: axon to axon
dendrodendritic: dendrite to dendrite

53
Q

electrical synapses

A

pre-synaptic neuron to postsynaptic neuron
-Action potential (axon) to graded potential (dendrite)
-Gap junction- very tight allowing ions flow from one neruon to other

54
Q

chemical synapse: presynaptic neuron

A

conducts action potential toawrds synapse

55
Q

chemical synapse: postsynaptic neruon

A

neruon whose signals are propagated away from the synapse

56
Q

chemical synapse: synaptic vesicles

A

stores neurotransmitter (carries signal across a synpse)

57
Q

chemical synapse: secretory granules

A

large vesicles that stores proteins

58
Q

chemical synapse: synaptic cleft

A

space between the presynaptic and postsynaptic neurons (10x wider than gap junctions)

59
Q

chemical synpase- steps

A
  1. action potential arrives at terminal
    2.triggers release of neurotransmitter from synapstic vesicle
    3.neurotransmitter migrates across synaptic celft
  2. binds with receptor on postsynaptic neuron
  3. graded potential is triggered
  4. neurotransmitters quickly removed from synaptic cleft
60
Q

The neuromusclar junction

A

synaptic junction onto muscle
-one of the largest synapse in the body
-fast and reliable
-large number of active zones aligned with folds in the motor end-plate
-much easier to study

61
Q

generation of an EPSP

A

Na+ flos from synaptic cleft into the cell
depolarization- more likely to have an AP

62
Q

generation of an IPSP

A

CL- flows from synpatic celft into the cell
hyperpolarization- less likely to have an AP

63
Q

Do neurons just have on connection?

A

No- neurons typically undergo many EPSPs and IPSPs from different axon terminals
Some neurons have up to 200 000 terminals

64
Q

What is required for a molecule to be considered a neurotransmitter

A
  1. Must be present within the presynaptic neuron
    2.Must be released in response to a presynaptic depolarization
  2. specific receptors must be present on the postsynaptic neuron
65
Q

Neurotransmitters require mechnisms to..

A

-be synthesized in presynaptic neuron
-loaded into the synaptic vesicles
-spilled out into the synaptic cleft (ie exocitosis)
-Bind with the postsynaptic neuron and create a response
-Be removed (reuptake and degradation)
** All needs to happen in miliseconds

66
Q

Neurotransmitters and synaptic drug interactions: possible drug interactions

A

-Altering the synthesis, transport, storage or release of a neurotransmitter
-modifying neurotransmitter interaction with the postsynaptic receptor
-influencing neurotransmitter reuptake or destruction

may also replace a neurotransmitter with a binding subsitute (agonist or antagonist)

67
Q

Small mollecule neurotransmitters

A

synaptic vesicles
4 broad groupings:
Acetylcholine, amino acids, purines, amines

68
Q

Peptide neurotransmitters

A

secretory granules
larger, slower

69
Q

Acetylcholine

A

used at the NMJ and synthesized by all motor neurons
-cholinergic neurons- synthesize acetylecholines
Also plays a major role in a number of autonomic activities in the brain

70
Q

acetylcholine enzymes: synthesis

A

choline acetyltransferase chAT

71
Q

acetylcholine enzymes: breakdown

A

acetylcholinesterase AChE

72
Q

Nerve gases (Sarin gas)

A

-inhibits acetylcholinesterase (AChE); ACh cannot be broken down from synaptic cleft (get constant ON state)
-can disrupt transmission on skeletal/heart muscle leading to death

73
Q

Dopamine

A

Part of amines group - more specifcially catecholamines
dopaminergic neurons synthesize dopamine

74
Q

how is dopamine synthesized (enzyme)

A

dopamine is synthesized from dopa with the enzyme dopa decarboxylase

75
Q

dopamine enzyme: breakdown

A

Monoamine oxidase-B (MAO-B) enzymes breakdwon dopamine

76
Q

what can happen if there is a lack of dopa

A

a lack of dopa can lead to the degradation and eventual death of some nerve cells int he brain (due to lack of signal because we can’t make dopamine)
-parkinson’s disease- tremors/ muscle rigidity

77
Q

PD-Levadopa

A

-Supplements reduced levels of dopa
-crosses blood brain barrier
-most effective treatment, but can wear off and has side effects

78
Q

PD- Dopamine agonists

A

-Mimics dopamine
-Good fisrt treatment but not as effective as levodopa (not great long term)

79
Q

PD- MAO-B inhibitiors

A

-blocks the reuptake of dopamine
-allows the limited dopamine to stay in the cleft longer

80
Q

Cocaine

A

blocks reuptake of neurotransmitter dopamine at presynaptic termials

81
Q

methamphetamine

A

Not only blocks reuptake of dopamine, but increases its release as well

82
Q

Meth and PD

A

-meth can lead to long term damage of dopaminergic neurons
-meth users are almost 2x as likely as non users to develop PD
-Still many other factors are presnt- but will PD rates continue to rise with rising rates of meth use?

KIN 3E03 (6 decks)

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