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Brain and Behavior Exam 1 > Lec 1 How the Brain is Different > Flashcards

Lec 1 How the Brain is Different Flashcards

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0
Q

Is there lymphoid drainage in the brain?

A

Nope! has CSF system instead

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1
Q

What is glial cell response to injury?

A

form scars not fibroblasts

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2
Q

How many neurons in the brain?

A

> 100 billion

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3
Q

What is embryo origin of neurons?

A

ectoderm

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4
Q

Can neurons be replaced?

A

No – after earliest days of infancy likely cannot be replaced

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5
Q

What is the perikaryon?

A

cell body of a neuron

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6
Q

What are the 3 main parts of the neuron?

A
  • cell body (perikaryon)
  • axon
  • dendrites
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7
Q

What is the receptive part of the neuron? The part that sends the output?

A
  • dendrites receive input

- axons send output to synapse

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8
Q

Are there more glial cells or neurons in the brain?

A

glial cells out-number neurons by 20x

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9
Q

What are the 4 types of glial cells?

A
  • astrocytes
  • oligodendroglia
  • ependymal cells
  • microglia
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10
Q

What type of glial cell makes of 20-50% of human brain volume?

A

astrocytes

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11
Q

What is embryonic origin of astrocytes?

A

ectoderm

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12
Q

What is function of astrocytes?

A
  • physical support (structural framework)
  • part of blood-brain barrier
  • supply glutamate to neurons
  • metabolic support (provide neurons with nutrients)
  • maintain ion balance in extracellular space (take up K that active neurons are releasing)
  • glycogen fuel reserve buffer (capable of glycogenesis, store and release glycogen for neurons to use)
  • repair nervous system
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13
Q

What 4 structures in the CNS/PNS come from the neuroectoderm?

A
  • CNS neurons
  • ependymal cells (inner lining of ventricles)
  • oligodendroglia
  • astrocytes
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14
Q

What 2 structures in CNS/PNS come from the neural crest?

A
  • PNS neurons

- Schwann cells

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15
Q

What structure in the CNS/PNS comes from the mesoderm?

A

microglia (M for Microglia, also Macrophages!)

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16
Q

Which parts of the neuron can be stained via the nissl substance? why?

A
  • cell bodies and dendrites can because nissl substance stains RER
  • RER is not present in the axon so axon does not stain
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17
Q

What marker is used to identify astrocytes histologically?

A

GFAP

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18
Q

What is the function of oligodendroglia?

A
  • myelinate axons of CNS neurons

- each cell myelinates ~30 axons

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19
Q

What is the main type of glial cells in white matter?

A

oligodendroglia

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20
Q

What is the embryological origin of oligodendroglia?

A

ectoderm

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21
Q

Which type of glial cells gives fried egg appearance on H&E?

A

oligodendroglia

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22
Q

What is histo appearance of ependymal cells?

A

epithelial like, ciliated, simple cuboidal

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23
Q

What is histo appearance of ependymal cells?

A

epethelial like, ciliated, simple cuboidal

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24
Q

What is function of ependymal cells?

A
  • line CSF-filled ventricles in brain and central canal of spinal cord
  • cilia on their apical surface help circulate CSF around
  • microvilli on their surface absorb CSF
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25
Q

WHat is the choroid plexus?

A
  • system of modified ependymal cells and capillaries that produce CSF
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26
Q

What is function of microglia?

A
  • macrophage of brain and spinal cord (CNS)
  • respond to parenchymal tissue damage / pathogens / toxins by differentiating into large phagocytotic cells and proliferating
  • phagocytoses neurons that undergo programmed death during development
  • no known function in resting state
  • monitor CNS environment and restore homeostasis after CNS injury
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27
Q

What is function of microglia

A

resident macrophage of brain and spinal cord

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28
Q

What is embryo origin of microglia?

A

mesoderm

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29
Q

What is histo shape of microglia in non-activated vs activated state?

A

non-activated: small irregular nuclei, little cytoplasm

active: large rod-shaped nuclei, bigger cyto

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30
Q

What is neuronophagia?

A

microglia encircle degenerating neurons

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31
Q

What happens to microglia with age?

A

– get progressively more activation in absence of stimulation

– may contribute to neurodegeneration that occurs in Alzheimer’s, Parkinson’s, HIV encephalopathy

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32
Q

What happens to microglia with age?

A

– get progressively more activation in absence of stimulation

– may contribute to neurodegeneration that occurs in alzheimers, parkinsons, HIV encephalopathy

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33
Q

What are the 3 ways the brain is sequestered by glial cells from rest of body?

A
  • blood-brain barrier
  • spatial buffering (maintenance of ion balance in extracellular fluid
  • active supervision of neuronal microenvironment
34
Q

What is the blood brain barrier?

A
  • controlled transcapillary transport

- prevents passage large molec from blood into interstitial fluid of CNS

35
Q

What 3 structures form the blood brain barrier?

A
  • endothelial cells lining capillary wall with tight junctions between them
  • astrocyte foot processes
  • capillary basement membrane
36
Q

What is unique about brain capillary endothelial cells?

A

Only brain capillary endothelial cells have tight junctions

37
Q

What is the blood-CSF barrier? made of?

A
  • prevents large molec passing from blood into CSF

- formed by tight junctions between epithelial cells of choroid plexus

38
Q

What are exceptions to the blood-brain barrier?

A
  • a few special regions have fenestrated capillaries and no blood-brain barrier so molec in blood can affect brain function
  • —– area postrema –> vomiting after chemo
  • —– OVLT –> osmotic sensing
    • in neurohypophysis no BB barrier so that ADH can be released from brain into circulation
39
Q

How much ox/glucose does brain need per minute?

A

500-600 ml oxygen

75-100 mg of glucose

40
Q

Where does energy for brain come from?

A
  • oxidative metabolism of glucose
41
Q

How much time deprived of oxygen will it take for neuron to die?

A

5-7 minutes

42
Q

List in order of most sensitive to anoxia (no oxygen)?
[most sensitive > least sensitive]

– astrocyte, axon, blood vessel, microglia, myelin, nerve cell (soma), oligodendroglial cell

A

nerve cell > axon > myelin > oligodendroglial cell > astrocyte > microglia > blood vessel

43
Q

What are 3 especially sensitive regions of CNS to anoxia?

A
  • neurons in cortical layers 3 and 5
  • hippocampus neurons (CA1 region, sommer’s sector)
  • purkinje cells of cerebellum
44
Q

What is eosinophilic degeneration? What happens to the cytoplasm? nucleus?

A
  • irreversible neuronal response to injury
  • perikaryal cytoplasm becomes eosinophylic (bright pink + homogeneous)
  • nucleus becomes pyknotic (dark and shrunken)
45
Q

When is eosinophilic degeneration visible?

A

4-6 hours after injury

46
Q

What is the axonal reaction? Histo appearance?

A
  • follows damage to or disease of the axon
  • may be reversible if integrity of axon restored
  • RER disintegrates
  • swelling and rounding of cell body
  • disappearance of Nissl substance
  • cytoplasm smooth (central chromatolysis)
  • peripheral migration of nucleus
47
Q

What is role of astroctyes in response to brain injury?

A
  • form glial scar comprised of reactive astrocytes
48
Q

What are the 3 steps of glial scar formation in response to brain injury

A
  1. Astrocytosis = astrocyte proliferate
  2. Reactive astrocytes form: cytoplasm swells and becomes eosinophilic
  3. gliosis: glial fibers in astrocytes coalesce and form glial scar made of GFAP [glial fibrillary acidic protein]
49
Q

Do fibrous (fibroblast) scars form in the brain in response to injury?

A

No –> glial scars are formed instead that are made of reactive astrocytes

50
Q

What is role of microglia in brain injury

A
  • proliferate and encircle degenerating neurons [neuronophagia]
  • form clusters around necrotic brain tissue
  • differentiate into macrophages –> go to site of damage and phagocytize debris associated with injury
51
Q

What is role of microglia in brain injury

A
  • proliferate and encircle degenerating neurons [neruonophagia]
  • form clusters around necrotic brain tissue
  • differentiate into macrophages –> go to site of damage and phagocytize debris associated with injury
52
Q

What is cerebral edema?

A
  • response to injury
  • increased water content or abnormal distribution of water in brain parenchyma (intracellular or extracellular spaces)
  • occurs with many acute pathologic processes
53
Q

What is vasogenic edema?

A
  • failure of tight junctions and astrocytic processes of blood brain barrier
  • allows normally excluded intravascular proteins/fluid to enter cerebral parenchymal extracellular space
54
Q

What is vasogenic edema?

A
  • failure of tight junctions and astrocytic processes of blood brain barrier
  • allows normally exluded intravascular protiens/fluid to enter cerebral parenchymal extracellular space
55
Q

How can you treat vasogenic edema?

A

steroids and osmotic therapy (mannitol)

56
Q

With what types of disease do you see vasogenic edema?

A
  • tumors, brain abscesses, traumas, inflammation, hypertension
57
Q

What is cytotoxic edema?

A
  • derangement in cellular metabolism causing failure of ATP-dependent Na/Ca transport
  • causes cellular retention of Na –> H20 folllows
  • astrocytic processes, capillary endothelial cells, and neurons swell –> cut off cerebral perfusion to adjacent areas so further hypoxic damage –> more cyto edema –> more cerebral swelling
  • can lead to potential herniation
  • BBB stays intact
58
Q

What is cytotoxic edema?

A
  • derrangement in cellular metabolism causing failure of ATP-dependent Na/Ca transport
  • causes cellular retention of Na –> H20 folllows
  • astrocytic processes, capillary endothelial cells, and neurons swell –> cutt of cerebral perfusion to adjacent areas so further hypoxic damage –> more cyto edema –> more cerebral swelling
  • can lead to potential herniation
  • BBB stays intact
59
Q

Does cytotoxic edema response to steroid or osmotic diuretics?

A

nope!

60
Q

What diseases is cytotoxic edema associated with?

A
  • early ischemia, hypoxia (cardiac arrest), asphyxia, various toxins
61
Q

Where do you see cytotoxic edema fluid on imaging?

A
  • involves astrocytes so see it in both grey and white matter
  • loss of grey-white matter interphase
62
Q

What are 5 clinical symptoms of increases intracranial pressure?

A
  • headache
  • nausea/vomiting
  • bradycardia
  • hypertension
  • loss of consciousness
  • papilledema (optic disc swelling)
63
Q

Why should you always consider brain CT or MRI before performing an LP?

A
  • occult CNS lesion can potentially produce herniation after LP
64
Q

What is the Monroe Kellie doctrine?

A
  • skull has fixed volume that contains brain/CSF/blood
  • if increase volume of one, need to compensate by decrease in volume of others OR an increase in intracranial pressure will occur
65
Q

What is equation for cerebral perfusion pressure?

A

CPP = MAP - ICP

cerebral perfusion pressure = mean arterial pressure - intracranial pressure

66
Q

What happens to CPP if high ICP (intracranial pressure)

A

CPP = MAP - ICP so if you increase ICP you will get lower CPP thus brain will have inadequate blood flow –> ischemia

67
Q

What are the 4 types of herniations

A
  • subfalcine herniation
  • transtentorial (uncal) herniation
  • central herniation
  • cerebellar/tonsillar herniation
68
Q

What is a subfalcine herniation?

A
  • cingulate gyrus is pushed laterally away from
    expanding mass and herniates beneath falx cerebri
  • seen with frontal masses
  • can compress anterior cerebral artery
69
Q

What is an uncal transtentorial herniation?

A
  • uncus of temporal lobe herniates down into posterior fossa through tentorial notch
  • can be terminal
70
Q

What is the uncus?

A

medial temporal lobe

71
Q

What are possible signs of uncal trantentorial herniation?

A
  • can be terminal unless ICP managed
  • compresses ipsilateral (on same side) CN III –> fixed and dilated pupil and “down and out” gaze
  • compress ipsilateral posterior cerebral artery –> contralateral homonymous hemianopsia = visual field loss on both eyes
  • compress contralateral crus cerebri –> causes ipsilateral paralysis = false localization sign
72
Q

What is a central herniation?

A
  • swelling of cerebral hemispheres causes to directly herniate down and cause bilateral uncal herniation
  • have sudden sever increased ICP –> can be especially lethal with young people because no room to accommodate increase brain swelling
73
Q

WHen do you see central herniation?

A
  • in young people with trauma, subarachnoid hemorrhage, meningitis
74
Q

What is cerebellar/tonsillar herniation?

A
  • tonsil of cerebellum herniates down through foramen magnum
  • due to increase ICP in posterior fossa (where cerebellum + brainstem are located)
  • rapidly can progress to terminal brainstem compression
75
Q

When do you see cerebellar/tonsillar herniation?

A
  • increased ICP in posterior fossa (cerebellum/brainstem) from mass, edema, bleed, etc)
76
Q

Symptoms of cerebellar/tonsillar herniation?

A
  • severe occipital headache, stiff neck, shoulder pain
  • papilledema (swollen eye disc)
  • rapidly causes terminal brainstem compression
77
Q

How does CSF flow?

A
  • produced by choroid plexus –> to lateral ventricles –> through inter-ventricular foramina –> to 3rd ventricle –> through cerebral aqueduct –> to 4th ventricle
  • exits ventricle system through foramina in 4th ventricle –> enters subarachnoid space and reabsorbed by arachnoid granulations
78
Q

What type of cells play role in inhibiting nerve regeneration?

A
  • glial cells , axons cannot grow across glial scar
79
Q

Can PNS regenerate?

A

yes!

80
Q

Where/when does neurogenesis occur?

A
  • mostly during pre-natal development
  • recently discovered adult neurogenesis continues in hippocampus and sub-ventricular zone (lining lateral ventricles)
  • hippocampal neurogenesis may be related to learning/memory, function not well known
81
Q

What does neuronal plasticity mean?

A
  • brain changes structurally/functionally with experience/activity
  • underlies longterm learning and memory
  • also mech of chronic pain and addition
82
Q

What is long-term potentiation (LTP)?

A
  • major mech of neuronal plasticity

- long-lasting enhancement in signal transmission between 2 neurons resulting from stimulation them synchronously

Brain and Behavior Exam 1 (15 decks)

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