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Clinical Neuroscience > module 1 > Flashcards

module 1 Flashcards

1
Q

what is the resting membrane potential

A

the constant voltage across the membrane when the cell is at rest

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2
Q

what is the synaptic potential

A

a change in potential when neurotransmitters bind to a receptor that allows ions to flow across the neuronal membrane

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3
Q

what is an action potential

A

a nerve impulse or spike that travels along an axon

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4
Q

what are the two requirements for generating voltage difference across the cell membrane

A

concentration gradient
membrane is selectively permeable

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5
Q

how do ions move relative to the concentration gradient

A

from high to low concentration by diffusion

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6
Q

how are membranes selectively permeable

A

because there are ion channel proteins

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7
Q

what is the equilibrium potential

A

the force of diffusion is equal and opposite to the electrical force
- net movement of ions is zero
(does not look at number of ions)

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8
Q

what does the nernst equation describe

A

ionic flow based on electrochemical gradients

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9
Q

what does the GHK equation predict

A

the resting membrane potential (Vm) of a cell for multiple ions present in a cell

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10
Q

what is the relative permeability of an ion

A

the ease with which the ions moves across the membrane

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11
Q

at rest, what kind of channels can remain open and allow ions to diffuse in and out of the cell

A

leak channels (not gated)

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12
Q

what ion leaks out more than others

A

potassium

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13
Q

what is active to counter the leak of potassium ions

A

sodium-potassium ATPase pump

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14
Q

what is moved in and out of the cell with the Na-K ATPase pump

A

3 Na+ out
2 K+ in

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15
Q

why is ATP required for the Na-K pump

A

because the ions are moved against their gradient

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16
Q

what concentrations are kept stable because of the Na-K pump

A

ionic concentrations

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17
Q

what chloride transporter do immature neurons express

A

NKCC1

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18
Q

what does NKCC1 do

A

pumps chloride into neurons so immature neurons have a high concentration of chloride inside the cell and a low concentration of chloride outside the cell

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19
Q

how does the NKCC1 transporter depolarize the cell in immature neurons

A

GABA-A receptors open in response to binding of GABA which allows chlorine ions to flow down their concentration gradient from inside to outside the cell, which creates a more positive inside of the cell as negative ions leave, depolarizing it

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20
Q

does the NKCC1 transporter depolarize or hyperpolarize the cell

A

depolarize
easier to fire AP

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21
Q

what chloride transporter do mature neurons express

A

KCC2

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22
Q

what does KCC2 do

A

pumps chloride out of neurons so mature neurons have a low concentration of chloride inside the cell and a high concentration of chloride outside the cell

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23
Q

how does the NKCC2 transporter hyperpolarize the cell in mature neurons

A

GABA-A receptors open in response to binding of GABA which allows chlorine ions to flow down their concentration gradient from outside to inside the cell, which creates a more negative inside of the cell as negative ions flow in, hyperpolarizing it

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24
Q

does the NKCC2 transporter depolarize or hyperpolarize the cell

A

hyperpolarize
harder to fire AP

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25
Q

in an AP are voltage gated channels open or closed at rest

A

closed

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26
Q

in an AP what causes the cell to depolarize

A

AMPA receptors open and sodium ions flow in

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27
Q

in an AP what is the threshold voltage

A

the voltage at which voltage-gated sodium channels open

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28
Q

in an AP what happens when the cell reaches threshold voltage

A

sodium channels open and sodium ions flow into the cell to depolarize the cell to positive voltages

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29
Q

in an AP at positive potentials are sodium channels activated or inactivated

A

inactivate by the channel being blocked and ions not being allowed to flow through

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30
Q

what is the absolute refractory period in an AP

A

sodium channels are inactivated and cells cannot fire another action potential until the channels recover from inactivation

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31
Q

in an AP when are potassium channels activated

A

top of the curve when cell is at positive potentials

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32
Q

in an AP what happens when potassium channels are activated

A

potassium ions flow out of the cell and the inside of the cell becomes less negative, hyperpolarization

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33
Q

in an AP what is the relative refractory period

A

potassium ions continue to flow in and the membrane voltage can be more negative than the resting potential
AP can be fired if input is larger (bigger depolarization than original required)

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34
Q

do AP move forward or backward

A

AP can only move forward not backward

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35
Q

what are three roles of refractory periods

A
  1. limit the number of APs that a neuron can produce per unit time
  2. prevent re-excitation of the same membrane segment that was just excited
  3. prevents APs from propagating backward to their point of initiation
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36
Q

why cannot passive current flow conduction along an axon be used to transfer information over long distances

A

passive current flow along an axon decays with distance

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37
Q

what is the difference between passive and active current flow

A

active current flow along an axon shows a constant amplitude of the action potential assuming equal distribution of channels along the axon so it does not decay with distance

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38
Q

what is difference about the sodium channels in the nodes of ranvier

A

there are more of them

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39
Q

what is the role of myelin

A

increases conduction velocity

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40
Q

how do AP travel through nodes of ranvier

A

AP travels passively to the next node where it is regenerated (called saltatory conduction)

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41
Q

what does myelin do to the strength of an AP

A

maintains the strength of the impulse message as it travels down the axon

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42
Q

how does myelin provide protective insulation

A

due to its fatty protein coating

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43
Q

the brain and spinal cord contain 50% white matter that is made up of what

A

oligodendrocytes

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44
Q

how many axons does one oligodendrocyte wrap around

A

many

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45
Q

what anchors the layers of myelin together in the CNS

A

myelin basic protein (MBP)
proteolytic protein (PLP)

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46
Q

what are motor and sensory peripheral nerves myelinated by

A

schwann cells

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47
Q

how many axons does one schwann cell wrap around

A

a single peripheral axon

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48
Q

what is the relation between nodes of ranvier and schwann cells

A

each segment between nodes of ranvier is wrapped by a different schwann cell

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49
Q

how many schwann cells are needed to myelinate one long axon

A

multiple

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50
Q

what does blocking potassium channels do to AP

A

prolongs the AP because the cell is not able to repolarize and takes much longer to come back to resting membrane potential
-relative refractory period is much longer
-neuron needs smaller input to fire

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51
Q

what are the three cells contained in a CNS synapse

A

presynaptic neuron
astrocyte
postsynaptic neuron

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52
Q

what synaptic vesicles are able to be released

A

ones at the active zone
(there are many different pools of vesicles)

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53
Q

what is the active zone on a presynaptic end of a synapse

A

area on the presynaptic membrane where vesicles release occurs
- contains many proteins that participate in various aspects of synaptic vesicle release and recycling

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54
Q

what leads to vesicle fusion and release of NT

A

voltage dependent calcium channels open in response to depolarization and the inflow of calcium leads to vesicle fusion and release of NT

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55
Q

where are vesicles synthesized

A

in the soma and then transported to the presynaptic terminal where they are stored

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56
Q

how are vesicles transported to the presynaptic terminal

A

along microtubules
- motor proteins generate force by coupling ATP hydrolysis to conformational changes

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57
Q

what are microtubules

A

polymers of tubulin stabilized by tau proteins

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58
Q

what are vesicles tethered to the release sites by

A

SNARE complex made of synaptobrevin on the vesicle membrane and SNAP 25 and syntaxin on the plasma membrane

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59
Q

what events lead to membrane fusion and release of vesicle contents

A

calcium binds to synaptotagmin

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60
Q

what are the four types of glial cells

A

astrocytes
oligodendrocytes
schwann cells
microglial cells

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61
Q

what are the functions of astrocytes

A

only found in CNS
maintain chemical environment around neurons
end-feet surround capillaries and help form the BBB

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62
Q

what are the functions of oligodendrocytes

A

make myelin in the CNS

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63
Q

what are the functions of schwann cells

A

make myelin in the PNS
-important in regeneration of PNS neurons

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64
Q

what are the function of microglial cells

A

hematopoietic cells and like macrophages
scavenge and secrete cytokines at site of injury
number of microglia increases in injury

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65
Q

what is the role of astrocytes at synapses in the CNS

A

astrocyte secreted factors control different aspects of synaptic development and maturation

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66
Q

what do synapse-astrocyte interactions contribute to

A

synaptic plasticity

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67
Q

what do astrocytes do to neurotransmitters

A

remove neurotransmitters from synaptic cleft and stop communication

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68
Q

what kind of homeostasis are astrocytes essential for

A

ionic homeostasis
potassium and calcium balance

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69
Q

what are the three ways that neurotransmitters can be removed from the synaptic cleft

A

destruction by enzymes
reuptake by presynaptic neurons
removal by transporters on astrocytes surrounding the synapse

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70
Q

what enzyme is acetylcholine destroyed by in the synapse

A

acetylcholine esterase

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71
Q

what four NT have transporters embedded in the presynaptic membrane

A

serotonin
dopamine
NE
epi

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72
Q

what transporters transport glutamate to astrocytes to be converted to glutamine

A

excitatory amino acid transporters (EAAT) that are present on astrocytes

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73
Q

how is the action of glutamate released into the synaptic cleft terminated

A

by uptake into surrounding glial cells via EAATs

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74
Q

within glial cells, what converts glutamate to glutamine

A

glutamine synthetase

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75
Q

glutamine is taken up into nerve terminals and converted back to glutamate by

A

glutaminase

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76
Q

how is glutamate loaded into synaptic vesicles

A

via vesicular glutamate transporters (VGLUTs)

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77
Q

is removal of glutamate from the synapse slow or rapid

A

rapid

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78
Q

what do dendritic spines provide

A

compartmentalization
- large head connected by very thin neck serves to compartmentalize molecules to individual synapses

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79
Q

what kind of synapses do dual spines have

A

both excitatory and inhibitory

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80
Q

T or F: activation of one synapse can be selectively strengthened without influencing neighboring synapses

A

true

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81
Q

what does the dendritic spine neck do to resistance and kinetics of the cell

A

increases resistance and can change the kinetics of voltage change that is transmitted to the soma

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82
Q

when will extra-synaptic receptors have a response

A

only if NT spills out of synapse

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83
Q

can synapses on dendritic spines modulate each other

A

yes
synapses on the shaft of dendrites can modulate response from many upstream spines

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84
Q

what clusters receptors near signaling molecules

A

postsynaptic proteins form a scaffold

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85
Q

what four things are contained at a glutamate synapse postsynaptic density

A

receptors
scaffolding proteins (PSD 95, Homer, Shank)
signaling molecules (CamKinase II)
actin filaments

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86
Q

what is PSD important for

A

scaffolding protein that is important for signaling as well as holding the shape of spines

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87
Q

what causes summation of AP

A

convergence of hundreds or thousands of presynaptic inputs across the soma and dendritic spines leads to summation

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88
Q

as a result of summation across space and time, what does the membrane potential depend on

A

whether it reaches threshold

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89
Q

what are the two types of NT receptors

A

ionotropic
metabotropic

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90
Q

what type of receptors are GPCRs

A

metabotropic
- cascade of phosphorylation events and second messenger production
- slow

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91
Q

what is it called when the receptor itself is also the ion channel

A

ionotropic receptors
- fast

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92
Q

can G proteins bind to and activate ion channels

A

yes

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93
Q

what are three types of heterotrimeric G proteins

A

Gs
Gi
Gq

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94
Q

are AMPA receptors fast or slow and what ions do they flux

A

fast kinetics
flux only sodium ions

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95
Q

are NMDA receptors fast or slow and what ions do they flux

A

slow
flux both sodium and calcium ions

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96
Q

what are two types of ionotropic receptors

A

AMPA
NMDA

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97
Q

what are the steps in glutamate signaling

A
  1. glutamate released from presynaptic terminal
  2. NMDA receptors activated
  3. depolarization of postsynaptic terminal
  4. magnesium repelled from the pore of the channel
  5. NMDA receptor can flux calcium and sodium
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98
Q

what are two stores of calcium

A

flux through ligand gated or voltage gated ion channels

release from intracellular calcium stores (in ER and mitochondria)

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99
Q

what two ion channels releases calcium from intracellular stores

A

IP3 receptors
ryanodine receptors

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100
Q

what are two examples of effector proteins that calcium can affect

A

calmodulin
cam kinase II

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101
Q

what are four ways calcium can be brought down to normal levels

A

pumping it out of the cell by calcium pump using ATP

Na/Ca exchanger that transports Na in and Ca out

Ca pump on ER membrane that pumps Ca into intracellular stores and transports Ca into the mitochondria

binding by buffering proteins like calbindin

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102
Q

what are proteins phosphorylated by

A

protein kinases

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103
Q

what are proteins dephosphorylated by

A

protein phosphatases

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104
Q

what are the two layers of the dura mater

A

one layer that is fused with the skill
one layer that is fused to the arachnoid

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105
Q

is there space between the two layers of the dura mater

A

no except where they separate to form sinuses (sinuses filled with CSF)

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106
Q

which meninge layer has pain receptors

A

dura mater

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107
Q

does the arachnoid mater follow the inner layer of dura into the sulci

A

no
- results in a large space filled with CSF

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108
Q

what is the subarachnoid space

A

space between the arachnoid and pia mater that is filled with CSF and contains blood vessels and arachnoid trabeculae

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109
Q

what is the arachnoid trabeculae

A

made of cells and collagen and holds arachnoid and pia together as well as blood vessels

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110
Q

what do arachnoid granulations do

A

allow CSF to exit the subarachnoid space and enter the sinuses to eventually enter the bloodstream
(takes things out of the brain and back into circulation)

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111
Q

what is the pia mater

A

closely follows the surface of the brain and adheres to glia on the surface of the brain

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112
Q

what are the three meninge layers

A

dura, arachnoid, pia

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113
Q

what type of molecule can cross the BBB

A

hydrophobic molecules because BBB is a phospholipid bilayer

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114
Q

what are the capillaries in the CNS linked by

A

tight junctions

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115
Q

what are endothelial cells in the CNS surrounded by

A

pericytes and the basement membrane

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116
Q

what surrounds blood vessels in the CNS

A

astrocytic feet

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117
Q

can macrophages squeeze out of capillaries in the CNS

A

no because of the presence of tight junctions

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118
Q

how do astrocytes modulate blood flow

A
  1. mGlu receptors activate on the astrocyte surrounding the synapse
  2. intracellular Ca in astrocytes increases
  3. PLP (Ca dependent 2nd messenger) is activated and diffuses through the astrocytes
  4. PLP activates formation/release of prostaglandins and vasoactive compounds
  5. blood vessels respond by dilating
  6. blood flow to the area increases
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119
Q

what are two roles of astrocytes at the synapse

A
  1. removal of glutamate from the synaptic cleft
  2. ionic homeostasis (especially of K)
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120
Q

where is anterior circulation derived from

A

internal carotid artery

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121
Q

where is posterior circulation derived from

A

vertebral artery

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122
Q

what connects blood vessels from the L and R side of the brain

A

circle of willis

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123
Q

what does the circle of willis create

A

a redundant blood supply because it is a continuous structure connecting the blood vessels

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124
Q

what areas of the brain does the middle cerebral artery supply (MCA)

A

language areas, sensory and motor areas, cognition
(basal ganglia, cortex, lobes, midbrain)

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125
Q

what areas of the brain does the anterior cerebral artery supply (ACA)

A

frontal cortex
cognitive areas, sensory areas in frontal lobe

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126
Q

what areas of the brain does the posterior cerebral artery supply (PCA)

A

vision, thalamus related
mid brain, brain stem, occipital lobe

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127
Q

what parts of the brain does the basilar artery supply

A

pons, lower midbrain, thalamus, hypothalamus

128
Q

how are sinuses formed

A

separation of layer of dura

129
Q

where does the CSF from the sinuses eventually drain into

A

jugular vein

130
Q

what do arachnoid granulations act as

A

one way valves for CSF to flow from brain tissues to sinuses

131
Q

where is CSF produced

A

choroid plexus present in each of the four ventricles

132
Q

what happens as CSF passes from the arterial perivascular space through the substance of the brain

A

metabolic wastes and discarded proteins are rinsed into the perivascular spaces surrounding veins and perivascular fluid flows into the subarachnoid space/sinuses

133
Q

when does convective flow of CSF and interstitial fluid increase

A

during sleep when extracellular spaces expand

134
Q

how is blood supplied to the spinal cord

A

branches of aorta that form the vertebral and spinal arteries

135
Q

what are the highly vascularized areas of the brain whose capillaries do not contain the tight junctions of the BBB but instead are fenestrated (gap between endothelial cells)

A

circumventricular organs
(allows free exchange of molecules between blood and nervous tissue)

136
Q

what are the sensory areas of the circumventricular organs called

A

subfornical region
OVLT
area postrema

137
Q

what are the sensory areas of the circumventricular organs involved in

A

homeostatic functions like fluid/blood pressure balance, temperature, respiration, hunger (glucose levels)

138
Q

what are the secretory areas of the circumventricular organs called

A

pineal gland
median eminence
intermediate pituitary
posterior pituitary

139
Q

what are the secretory areas of the circumventricular organs involved in

A

neurosecretion of secrete hormones prolactin, growth hormones, oxytocin, feedback loops from rest of body

140
Q

when do surface electrodes of an EEG register a signal

A

when cells signal in synchrony

141
Q

what can ERP (event related potentials) be recorded from

A

EEG

142
Q

how do CT scans work

A

short pulses of narrow x-ray beam while detectors are placed across the brain that probe small portions of the tissue
radiodensity calculated at each point and complete image is generated

143
Q

how are images for a CT scan collected

A

as slices

144
Q

what is a drawback of a CT scan

A

high level of radiation

145
Q

what is PET imaging based on

A

the use of specific metabolites by active cells

146
Q

how does PET imaging work

A
  1. isotope of glucose injected by IV
  2. isotope accumulated in active neurons but cannot be metabolized
  3. as isotope decays, two positrons are emitted and travel in opposite directions
  4. gamma rays are produced
  5. positrons detected when they react with electrons
  6. positrons mapped onto a CT or MRI image
147
Q

what kind of diseases are PET scans used for

A

neurodegenerative diseases

148
Q

how does MRI imaging work

A
  1. protons lineup with magnetic field and will spin at a frequency that depends on the field strength
  2. when a brief radiofrequency pulse is applied, atoms are knocked out of alignment
  3. protons emit energy as they realign themselves with the magnetic field
    (no radioactive substance injected although a contrast is sometimes used)
149
Q

what are T1 weighted MRI images

A

produced by using a short time between successive radio frequency pulses
- grey matter appears darker than white matter

150
Q

what are T2 weighted MRI images

A

produced with a longer time in between successive radio frequency pulses
- white matter appears darker than gray matter
- signal of water is enhanced

151
Q

how does fMRI work

A

depends on hemoglobin molecule distorting the magnetic properties of hydrogen
- distortion depends on whether oxygen is bound to hemoglobin or not

152
Q

is the resolution of a fMRI better than a PET scan

A

better

153
Q

what is diffusion tensor imaging (DTI)

A

type of MRI that allows visualization of fibrous structures like large tracts of white matter

154
Q

what kind of disease is DTI useful for

A

multiple sclerosis

155
Q

what is a magnetoencephalography (MEG)

A

records the magnetic consequences of the brains electrical activity
- temporal resolution is milliseconds

156
Q

what is magnetic source imaging (MSI)

A

combines structural MRI with MEG

157
Q

what kind of scan has the highest anatomical resolution

A

fMRI
(can detect very small structures)

158
Q

what kind of scan has the highest sensitivity

A

PET
(can detect very low signals)

159
Q

what is the sensitivity and temporal resolution for a PET scan

A

highest sensitivity
low temporal resolution

160
Q

what is the spatial and temporal resolution for a EEG

A

low spatial resolution
high temporal resolution

161
Q

what is the sensitivity and spatial resolution for a MRI

A

good spatial resolution and sensitivity

162
Q

what is the spatial and temporal resolution for a fMRI

A

good spatial resolution
good temporal resolution

163
Q

what will symptoms of a stroke depend on

A

the artery that is blocked/hemorrhaging

164
Q

what is the most significant risk factor for a stroke

A

hypertension

165
Q

what is a CVA

A

cerebrovascular incidence (CVA) is a stroke
- occurs when there is obstruction of blood flow

166
Q

what is a TIA

A

transient ischemic attack (TIA)
- sxs last less than 24 hours

167
Q

what is the difference between a TIA and a stroke

A

a stroke has symptoms that last for more than 24 hours

168
Q

what are the two main categories of strokes

A

ischemic strokes: caused by blockage of an artery
hemorrhagic strokes: caused by bleeding

169
Q

what is an ischemic stroke

A

occurs when a blood vessel that supplies the brain becomes blocked or clogged and impairs blood flow to that part of the brain
- brain cells and tissues begin to die within minutes forming a cerebral infarct

170
Q

what are the two types of ischemic strokes

A

thrombotic strokes: caused by a blood clot that develops in blood vessels inside the brain

embolic stroke: caused by a blood clot/plaque debris that develops elsewhere in the body and then travels to one of the blood vessels in the brain through the bloodstream

171
Q

what is a global ischemic stroke

A

caused by global decrease in blood due to cardiac arrest, valvular heart disease, or lowered blood pressure

172
Q

what is a hemorrhagic stroke

A

occurs when a blood vessel ruptures and bleeds
- cells/tissues do not get oxygen and nutrients
- pressure builds in surrounding tissues and irritation and swelling occur

173
Q

what are the two categories of hemorrhagic stroke

A

intracerebral hemorrhage: bleeding from blood vessels in brain

subarachnoid hemorrhage: bleeding in subarachnoid space, most commonly as result of bleeding aneurysm

174
Q

what are four things that can cause hemorrhagic strokes

A

chronic hypertension
congenital aneurysm/AVM
TBI
cocaine/amphetamine

175
Q

how does blood accumulate in the meninges to form a hemotoma

A

rupture of blood vessels

176
Q

where is an epidural hematoma and what is it caused by

A

blood between skull and dura that has peeled off
due to injury

177
Q

where is a subdural hematoma and when is it common

A

blood between dura and the brain
common in old age

178
Q

what causes cerebral edema after a stroke

A

large influx of CSF may drive swelling
- depolarization of injured and swollen tissue is also seen

179
Q

what is a severe complication of an acute ischemic stroke

A

cerebral edema

180
Q

during ischemia, why does excessive fluid accumulate in the intracellular or extracellular spaces of the brain

A

failure of energy-dependent ion transport
destruction of BBB

181
Q

what is the treatment for edema that cannot be treated with medication

A

decompressive craniectomy

182
Q

what is atherosclerosis

A

narrowing of blood vessels due to accumulation of plaques
- reduces blood flow especially in small end-capillaries

183
Q

what do plaques have high levels of

A

calcium, fatty acids, triglycerides, cholesterol

184
Q

what are plaques covered by

A

a fibrous cap of collagen that is typically weak and prone to rupture

185
Q

what does the cap of a plaque form if it enters the bloodstream

A

thrombus

186
Q

where is a thrombus most likely to block blood flow

A

branch points and atherosclerotic capillaries

187
Q

how is the clotting cascade activated

A

by collagen or injury to blood vessels

188
Q

what is the order of the clotting cascade

A

activation of thrombin
–> thrombin catalyzes conversion of fibrinogen to fibrin
–> fibrin forms crosslinks to form a clot

189
Q

what do blood clots contain

A

meshwork of platelets covered by crosslinked fibrin

190
Q

atherosclerosis combined with hypertension increases what risk

A

risk of stroke

191
Q

what is a medication that helps prevent platelet aggregation and is prescribed to patients at risk of stroke

A

NSAIDs (non steroidal anti inflammatory drugs)

192
Q

what medications prevent fibrin from forming

A

heparin and coumadin (blood thinners)

193
Q

can the core of the infarct be rescued after the fact

A

no, the cells are dead

194
Q

what is the penumbra

A

cells surrounding the primary lesion of the stroke

195
Q

can the penumbra be recovered after the fact

A

it is possible to limit stroke damage with quick reperfusion because restoring blood supply to the penumbra can help unhealthy cells recover and limit stroke injury to the core

196
Q

what two important metabolites does the blood carry for the brain

A

glucose and oxygen

197
Q

how does the brain use ATP

A

for the Na/K pump to maintain ion gradients
vesicular release and recycling at presynaptic terminals

198
Q

what does constant synthesis of ATP require

A

both glucose and oxygen

199
Q

what kind of cellular respiration can neurons perform

A

aerobic cellular respiration (with oxygen)
- need constant oxygen for oxidative phosphorylation

200
Q

does brain tissue store glucose

A

no
- also lacks ability to break down fatty acids

201
Q

why does the brain need a constant supply of glucose and oxygen

A
  1. the brain cannot store glucose in any form that is able to be broken down when the brain needs it
  2. neurons can only do aerobic respiration (no anaerobic)
202
Q

what is the only way neurons can get ATP

A

breakdown of glucose using aerobic cellular respiration

203
Q

what happens to the brain in relation to glutamate when there is no ATP

A

excitotoxicity
- astrocytes usually take up glutamate from synapse but without ATP they cannot so glutamate leaks out of the synapse to keep exciting neurons

204
Q

what happens to cell death signaling when there is no ATP

A

cell death increases

205
Q

what happens to the brain in relation to mitochondria when there is no ATP

A

mitochondrial dysfunction leads to the production of reactive oxygen species which will make proteins misfold/kill everything they encounter

206
Q

why does inflammation occur when there is no ATP in the brain

A

when the BBB breaks down, immune cells cross the BBB and cause neuroinflammation

207
Q

what are the differences between necrosis and apoptosis

A

necrosis:
passive, uncontrolled, and accidental cell death
cell bursts, contents released, microglia come to clean up contents, INFLAMMATION

apoptosis:
programmed cell death
tightly regulated active ATP-dependent process, forms vesicles for microglia to clean up, NO INFLAMMATION

208
Q

how does apoptosis occur

A
  1. mitochondria release pro-apoptotic proteins like cytochrome c
  2. cytochromes activate caspases (enzymes that destroy cellular proteins)
  3. DNA fragments and membrane integrity is maintained so cellular contents don’t spill out
  4. apoptotic bodies are cleaned up by macrophages/microglia
209
Q

what are the most sensitive cells to anoxic injury

A

neurons

210
Q

what is liquefactive necrosis

A

occurs in the brain as many macrophages clean up the necrotic cellular debris

211
Q

what scan gives the most detail of an ischemic stroke

A

MRI

212
Q

how many days after a stroke does the penumbra stay viable

A

two days

213
Q

what is the difference between diffusion-weighted images and perfusion images of an MRI

A

diffusion-weighted images: show structural (permanent) destruction

perfusion images: show areas where the brain has abnormally low perfusion (flow)

214
Q

what is inserted into the femoral artery to visualize both arteries and veins

A

contrast media
- can cause stroke, allergic reactions, and cause renal failure

215
Q

why are blood thinners a treatment for stroke

A

they block the clotting cascade

216
Q

what are three stroke treatments

A
  1. restore blood flow by removing the clot or stopping the hemorrhage
  2. protect neurons
  3. rehabilitation
217
Q

how can a blood clot be dissolved/lysed

A

perfusing tissue plasminogen activator (tPA)

218
Q

what are three treatments for excitotoxicity because of decreased ATP

A
  1. glutamate receptor antagonists
  2. block calcium signals
  3. bind and remove ROS/NOS
219
Q

how do neurons in the core of the infarct die

A

necrosis

220
Q

how do neurons in the penumbra die

A

apoptosis

221
Q

how can hypothermia be used for strokes

A

reduces cell death, injury, and edema

drawbacks are risk of pneumonia or arrhythmia

222
Q

how can atherosclerosis be treated

A

a balloon angioplasty and a stent is placed

223
Q

why is rehabilitation essential for recovery from a stroke

A

causes plasticity of neurons, reduction in swelling, dendritic sprouting

224
Q

what is the critical period after a stroke where rehabilitation is most effective

A

60-90 days

225
Q

what do intracellular buffer proteins do when Ca activates them

A

binds to downstream targets when activated by Ca

226
Q

what does the calcium pump require in order to pump Ca out of the cell

A

ATP

227
Q

what are four things that contribute to the mitochondria’s role in excitotoxicity

A
  1. pro-apoptotic proteins on mitochondrial membrane are activated
  2. cytochrome c –> activation of caspases (enzymes that lead to apoptosis)
  3. ROS –> membrane lipid breakdown
  4. increased intracellular calcium
228
Q

what leads to formation of pores in mitochondrial membranes

A

hypoxia

229
Q

in the absence of cellular respiration and lack of ATP, what happens to the mitochondria

A

they get depolarized

230
Q

what kind of ischemic strokes are considered focal ischemic strokes

A

thrombotic strokes
embolic strokes
(global ischemic strokes are not and make up 10% of ischemic strokes)

231
Q

what is TBI

A

physical injury to the brain or spinal cord

232
Q

what scale is used to assess the extent of a traumatic brain injury

A

glasgow coma scale

233
Q

what number is worse on the glasgow coma scale

A

lower number is worse
(does not respond to stimulus is worse than is in extreme pain)

234
Q

what are the two kinds of injury that TBIs can be divided into

A

primary injury: injury caused by the initial force
secondary injury: consequences of primary injury

235
Q

what is the difference between the coup and the counter-coup in a TBI

A

coup: side of contact; injury will be the same if the head is stationary and hit by moving object or vise versa

counter-coup: rebound effect on the opposite side

236
Q

what can shear forces of a TBI cause

A

vascular injury: blood vessels can break and become leaky causing hemorrhage, hematoma, or ischemia downstream of the break or leak

diffuse axonal injury: axons and dendrites break or have leaky membranes causing demyelination, neuronal injury, depolarization, lack of ATP, excitotoxicity

236
Q

what is reactive gliosis

A

change in glia after any injury (including stroke)

236
Q

what are the shear forces in a TBI

A

forces on axons in the spinal cord or brain which can break

237
Q

how do astrocytes react to injury

A

increasing their cytoskeleton and advancing thick processes towards the injury
multiplying
releasing extracellular matrix molecules

237
Q

what do reactive astrocytes form

A

a scar that limits inflammation and regulates composition of extracellular fluid

238
Q

what does brain injury do to glia in relation to regrowth

A

brain injury elicits responses from activated glia that actively opposes regrowth

239
Q

what forms the glial scar

A

overgrowth of the 3 activated glia
- accompanied by a massive influx of immune cells including T-cells, neutrophils, and monocytes

240
Q

what do scarring astrocytes form around the injury

A

form a capsule

241
Q

what is a mature glial scar a barrier to

A

the regrowth of axons across the site of CNS damage
- also have molecules on their surface that bind to receptors on newly generated axons and inhibit growth

242
Q

what is axonal sprouting

A

formation of new processes
- is unsuccessful because of the glial scar
- want to prevent random synapses from forming and working against new formation

243
Q

what kind of protein deposits are found after a TBI

A

hyperphosphorylated Tau proteins (like found in alzheimers patients)

244
Q

what happens to the microtubules when Tau proteins are phosphorylated

A

microtubules will break because the tau proteins are no longer stabilizing them

245
Q

are spinal and cranial nerves part of the CNS or PNS

A

PNS

246
Q

where is the white matter located in the spinal cord

A

white matter is outside
- axons are more susceptible to injury

247
Q

where is the white matter located in the brain

A

white matter is on the inside, grey matter is on the outside
- neurons are more susceptible to injury

248
Q

where do sensory axons enter the spinal cord and when do they cross to the other side

A

enter from skin and pain receptors

immediately decussate (cross over to the contra-lateral side)

249
Q

where will the loss of pain occur when there is injury to the spinal cord

A

injury to spinal cord will have contralateral loss of pain

250
Q

where do motor axons enter the spinal cord and when do they cross to the other side

A

enter from the motor cortex in the brain and travel to the medulla

decussate in the medulla before entering the spinal cord

251
Q

where will motor control be lost when there is injury to the spinal cord

A

injury to the spinal cord will have ipsilateral (same side) loss of motor control

252
Q

what kind of loss will stroke/brain injury in the corticospinal (motor) tract result in

A

contralateral loss

injury to the spinal cord will be ipsilateral

decussates in the medulla

253
Q

what kind of loss will occur with injury to the spinothalamic tract (pain)

A

contralateral
decussates right away

254
Q

what kind of loss will occur with injury to the dorsal column (touch)

A

ipsilateral loss

decussates in the medulla

255
Q

what can molecules released by oligodendrocytes and astrocytes actively suppress after injury

A

axonal regeneration

256
Q

what are the 4 major cellular elements that facilitate peripheral nerve repair

A

schwann cells
fibroblasts
macrophages
endothelial cells

  • all 4 required for formation of a nerve bridge
257
Q

what are the steps after injury that cause a channel promoting growth to form

A

injury
immune cells proliferate and invade
demyelination
form a nerve bridge
blood vessels extend into the site
schwann cells proliferate
channel forms that promotes growth

258
Q

what are three things that are prevented around the injury to protect cells during long term treatment

A

prevent excitotoxicity
prevent edema
prevent inflammation

259
Q

how can treatment be used to promote repair after an injury

A

using artificial biomaterials to promote regeneration in the spinal cord

  • stem cells obtained from nasal epithelium and other sources
  • drawback: not specific and no control over where progenitor cells end up
260
Q

what are 3 physical/occupational therapies combined with nerve stimulation that can be used in the long term treatment of brain injury

A

robot assisted locomotor training
functional electrical stimulation (FES) devices
repetitive transcranial magnetic stimulation (rTMS)

261
Q

what are 3 experimental therapies being used for brain injuries

A

masking ligands/receptors that inhibit axonal growth (antibodies against NogoA mask it and prevent its action)
blocking rho (rho collapses the growth cone)
hypothermia

262
Q

what is the difference between afferent and efferent

A

afferent: sensory information sent to the CNS (PNS–> CNS)

efferent: motor commands send to the PNS (CNS–>PNS)

263
Q

what kind of information is somatosensory information

A

sensory information such as touch, pain, proprioception

264
Q

what kind of information is visceral sensory information

A

sensory information that senses physiology like blood pressure

265
Q

where are neuronal cell bodies located that have modified nerve endings that form touch and pain receptors on the skin

A

dorsal root ganglia

266
Q

what is a detmatome

A

innervation arising from a single dorsal root ganglion and its spinal nerve

267
Q

how can spinal lesions be localized

A

by determined which dermatomes are affected

268
Q

how does pain information get from pain receptors to the somatosensory cortex and other pain centers

A
  1. pain and temperature fibers enter the spinal cord
  2. decussate in the same segment (cross over to the other side of the spinal cord)
  3. travel to the contralateral somatosensory cortex
269
Q

what tract are pain and temperature fibers a part of

A

the anterolateral tract

270
Q

how does touch information get from touch receptors to the somatosensory cortex

A
  1. touch fibers enter the spinal cord
  2. travel ipsilaterally in the dorsal column
  3. decussate in the medulla
  4. go to the contralateral somatosensory cortex
271
Q

what is the difference between the location of the dorsal columns and the anterolateral tracts

A

dorsal columns: midline

anterolateral tracts: outer edge of the spinal cord

272
Q

what pathway do mechanoreceptors and proprioceptors travel to the brain

A

dorsal column

273
Q

what pathway do nociceptors and thermoreceptors travel to the brain

A

spinothalamic tract
/ anterolateral tract

274
Q

how do motor axons travel from the brain to the spinal cord

A

as bundles along the pyramidal tract

275
Q

what is the difference between the lateral corticospinal tract and the anterior corticospinal tract in the efferent motor pathway

A

lateral: fibers decussate in medulla (90%)
anterior: fiber stay ipsilateral (10%)

276
Q

what kind of paralysis will a lesion of lateral corticospinal tract result in

A

ipsilateral paralysis

277
Q

where will the loss of touch and pain be for a lesion on the left side of the spinal cord

A

loss of touch on the left
loss of pain on the right

(loss will be below the segment that is lesioned)

278
Q

what is referred pain

A

visceral (internal) pain that is perceived at a site different from where it originated

279
Q

how is referred pain transmitted

A

via dorsal horn neurons that also convey cutaneous pain

280
Q

how does visceral pain travel

A

via the dorsal column
- afferent fibers decussate in the medulla

281
Q

what nervous system includes the enteric nervous system

A

autonomic nervous system

282
Q

what do the axons look like / where are the neurons located in the sympathetic nervous system

A

chain of sympathetic ganglia runs along the spinal cord
short preganglionic
long postganglionic

283
Q

what do the axons look like / where are the neurons located in the parasympathetic nervous system

A

parasympathetic ganglia are close to target organ
long preganglionic
short postganglionic

284
Q

what is the difference between the direct and consensual pupillary response

A

direct: bright light is shone, pupillary muscles contract, pupil becomes small

consensual: pupillary muscles of other eye contract at the same time

285
Q

what is the circuit that is responsible for the pupillary light reflex

A
  1. light activates optic nerve
  2. optic nerve fibers project bilaterally to the pretectum
  3. pretectum projects bilaterally on the edinger-westphal nucleus
  4. axons from edinger-westphal nucleus form part of cranial nerve 3 and terminate on ciliary ganglia
  5. ciliary ganglia have short axons and terminate on pupillary muscle
  6. constriction of pupils (parasympathetic response)
286
Q

what is the difference between seizures and epilepsy

A

seizures: uncontrolled synchronous firing of neurons in brain that cause behavioral abnormalities

epilepsy: clinical syndrome with recurrent, unprovoked unpredictable seizures (usually has underlying cause)

287
Q

what is the prodromal phase of a seizure

A

knowing the seizure is on its way
- lightheaded, anxiety, mood changes

288
Q

what is the aura phase of a seizure

A

early phase
- odd smell, sound, taste, vision problems

289
Q

what is the ictal phase of a seizure

A

time from the first symptom to the end
- intense electrical activity

290
Q

what is the post ictal phase of a seizure

A

recovery but physical symptoms are present

291
Q

what is the best way to diagnose a seizure

A

EEG

292
Q

what are focal seizures

A

start in/on one part or side of the brain and symptoms depend on the focus (what part of the brain it is in)

293
Q

what is the difference between a seizure with dyscognia and without

A

with dyscognia: cognitive impairment and often come with aura

294
Q

what is the difference between a focal and a generalized seizure

A

generalized seizure involve the entire brain

295
Q

what are absence seizures

A

appear as if person is spaced out

296
Q

what are atonic seizures

A

loose muscle tone suddenly

297
Q

what are myoclonic seizures

A

sudden contraction of a set of muscles (sudden jerky movement)

298
Q

what are tonic-clonic seizures

A

contractions of entire body, increased heart rate and BP

299
Q

what are status epilepticus

A

seizures last longer than 5 minutes

300
Q

what are 5 factors that can lead to an epilepsy diagnosis

A
  1. epilepsy syndrome: multiple factors that can lead to epilepsy
  2. idiopathic epilepsy: cause not known
  3. genetic
  4. acquired epilepsy: due to head trauma
  5. drug abuse
301
Q

what are two main ways to cause repetitive firing of action potentials by a neuron

A
  1. shorten absolute refractory period by changing when the Na inactivation protein blocks the channel
  2. shorten the relative refractory period by causing K+ channels to not hyperpolarize the cell as much
302
Q

what is a quantum

A

neurotransmitter contained in one vesicle

303
Q

where on the neuron is it decided if the potential is enough to cause an AP

A

at the axon hillock

  • EPSP and IPSPs can cancel each other out as long as the potential at the axon hillock is enough to cause the AP to fire
304
Q

what are basket cells

A

interneurons that contribute to the negative feedback loop

305
Q

what are pyramidal cells connected by

A

gap junctions - forming electrical synapses
- one firing will lead to another firing because they are electrically connected (rhythmic pacemaker cells)

306
Q

what are mossy fibers

A

axons of granule cells that project to CA3 pyramidal neurons, neurons in the hilus, and interneurons

307
Q

what do mossy fibers do in some epilepsy

A

sprout new fibers and make more connections

308
Q

what is epileptogenesis

A

period of structural and functional changes when symptoms are still absent

309
Q

where in the brain does mesial temporal lobe epilepsy (MTLE) cause damage

A

hippocampus

310
Q

why are children more prone to epilepsy

A

because they have immature neurons that express NKCC1 so there is higher Cl- inside cell, making it easier to excite the cell since it is already depolarized

311
Q

what are three main categories of drugs used as treatment for epilepsy

A

enhance GABA action
Na2+ channel blockers
Ca2+ channel blockers

312
Q
A

Clinical Neuroscience (4 decks)

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