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Clinical Neuroscience > Cumulative Final Questions > Flashcards

Cumulative Final Questions Flashcards

1
Q

What is the sequence of events involved in transmission at a typical chemical synapse?

A
  • -> depolarization of presynaptic terminal causes opening of voltage-gated Ca2+ channels
  • -> Ca2+ causes vesicles to fuse with presynaptic membrane
  • -> NT is released into synaptic cleft via exocytosis
  • -> NT binds to postsynaptic receptors
  • -> Removal of NT by glial uptake or degradation
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2
Q

What are the steps for activation of G-proteins?

A
  1. Signal binds to receptor
  2. Conformational change in receptor
  3. GDP is exchanged for GTP
  4. a-subunit dissociated from B and goes off to do work in the cell
  5. GTP on the a-subunit is hydrolyzed to GDP (“turning off”)
  6. GDP bound a-subunit associated with B subunit and binds to receptor
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3
Q

What is the regulation of GPCRs?

A

GAP: turns off G-protein
GEF: turns on G-protein

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4
Q

In the simplest terms, what is a stroke?

A

Disruption of blood flow to the brain

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5
Q

What is an ischemic stroke?

A

Insufficient blood supply cause by a blood clot

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6
Q

What is thrombotic?

A

Buildup in cerebral blood vessel

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7
Q

What is an embolus?

A

A circulating clot that blocks blood from going to the brain

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8
Q

What is a hemorrhagic stroke? What are the consequences?

A

Bleeding inside the skull due to a rupture in an artery. Results are contralateral paralysis and disruption to white matter

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9
Q

How does a hemorrhagic stroke vs. an ischemic stroke appear on a CT scan?

A

Hemorrhagic stroke large white density, ischemic stroke is darker

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10
Q

What is the penumbra?

A

Region surrounding the core infarct region of the stroke in which some residual blood flows remains. Tissue is still viable and salvageable

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11
Q

Why is the role of glia affected during a stroke?

A

Astrocytes take up glutamate from the synapse, but without any energy the astrocytes can’t take up the extra glutamate which leads to excitotoxcity

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12
Q

What is tPA?

A

Protease that cuts fibrin and degrades fibrinogen to dissolve a clot

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13
Q

What is the brainstem made up of? What are its main functions?

A 
Brainstem = midbrain, pons, medulla 
Main functions 
-Receive most cranial nerves
- Throughway for ascending sensory tracts and descending motor tracts
-Reticular formation
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14
Q

What is the cellular response to injury in the PNS?

A

Neurons of the PNS regenerate quite well because Schwann cells stimulates growth factors

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15
Q

What is the cellular response to injury in the CNS?

A

CNS neurons do not regenerate well. Oligodendrocytes release NogoA that causes the collapse of growth cones and inhibits growth. Astrocytes form a glial scar

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16
Q

Describe the phases of an action potential

A
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17
Q

What are the postsynaptic responses mediated by ionotrophic glutamate receptors - NMDA & AMPA?

A

Ionotrophic AMPA receptors open faster than NMDA receptors, allowing Na+ influx which depolarizes the membrane. This causes Mg2+ to be released from the NMDA channel and then NMDA receptors allow cations to flow

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18
Q

What does ictal mean? Interictal?

A 
Ictal = seizure 
Interictal = time between seizures
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19
Q

What are the 2 main types of seizures? What are the differences in each?

A

Generalized seizures: uncontrollable discharge of neurons in both hemispheres
Focal seizure: abnormal activity involving only a small part of the brain

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20
Q

Why are babies prone to having seizures?

A

In the developing brain, intracellular Cl- is higher making it want to leave the cell and depolarize causing GABA to be excitatory

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21
Q

What are 2 examples of mutations that could lead to epilepsy?

A

Blocking a K+ channel & activating a Na+ channel

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22
Q

What are the 3 major categories of AED drugs?

A
  1. Enhance GABA action
  2. Nat+ channel blockers
  3. Ca2+ channel blockers
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23
Q

What are the 3 degrees of neurons in the touch pathway?

A 
1*= periphery to medulla 
2* = medulla to thalamus (cross midline in medulla) 
3*= thalamus to SS cortex
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24
Q

What are the 3 degrees of neurons in the pain and temperature pathway?

A

1= periphery to spinal cord
2=spinal cord to thalamus (cross midline in spinal cord)
3*= thalamus to SS cortex

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25
Q

What happens in demyelinated axons?

A

When axons are demyelinated, the membrane is leaky so the current dissipated and there is not enough depolarization to reach threshold at the next patch of Na+ channels.
Axonal transport along microtubules is disrupted by Ca2+ and this can cause organelles to aggregate

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26
Q

What is Multiple Sclerosis (MS)?

A

A chronic progressive neuroinflammatory disease that damages myelin and neurons in the brain & spinal cord

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27
Q

What are the different T helper cells involved in MS disease progression? What do they do?

A

CD4+ : release pro-inflammatory cytokines that attract macrophages and microglial cells
CD8+ : kill oligodendrocytes

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28
Q

What is the role of B cells in MS progression?

A

B cells are antibody producing cells of the immune system made in bone marrow

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29
Q

Why would a K+ channel blocker be effective in MS?

A

K+ channels blocked broadens the action potential due to slower repolarization. This allows current to jump across a demyelinated segment

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30
Q

Why would a Na+ channel blocker be effective in MS?

A

In MS after neurons are demyelinated, there are more sodium channels expressed and this can lead to persistent influx of Na+ ions, therefore the Na+/K+ atpase need to work harder to pump Na+ out. Na+ channel blockers help prevent Na+ influx in neurons

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31
Q

What happens in ALS?

A

Both the UMN and the LMN degenerate or die and stop innervating muscles.

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32
Q

What is the pathology of ALS?

A

As LMNs begin to die –> sprouting of other LMNs and aberrant activity (causes fasciculations & twitches)

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33
Q

What do you see in the cellular pathology of ALS patients?

A

Stress granules found in the cytoplasmic inclusion bodies of UMN. The granules contain TDP-43 aggregates and often become a target for ubiquitination. If a patient has SOD1 mutations then see aggregated SOD1 in stress granules.

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34
Q

What are the genes that cause an increased risk for ALS if mutated?

A

SOD1, FUS, TDP-43, C9orf72

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35
Q

What is cell non-autonomous?

A

A trait in which genotypical mutant cells can cause other cells to exhibit a mutant phenotype

36
Q

What is the direct pathway of the basal ganglia?

A

Direct –> striatum (+), MSN (-), GPi (-), Thalamus (+)

37
Q

What is the pathology of PD?

A

Loss of DA neurons in substantia nigra & over-expression of the alpha-synuclein protein leads to beta sheet confirmation and aggregates called Lewy bodies

38
Q

What are the genetic risk factors for PD?

A

alpha-synuclein, Parkin, PINK1

39
Q

How is autophagy affected in PD?

A

Normal Parkin and PINK1 act together to remove failing mitochondria from cells

40
Q

What are the goals for treatment of PD?

A

Drugs that increase DA in striatum

41
Q

What do Levodopa and carbidopa do?

A

Dopamine doesn’t cross the BBB, so give L-DOPA as a precursor. Carbidopa is a peripheral DOPA decarboxylase inhibitor so more DOPA crosses the BBB

42
Q

What is the cause of HD?

A

Inherited monogenic disorder: tri-nucleotide repeat disease. The htt gene encodes HTT proteins, a CAG repeat in the htt gene causes extra glutamine in the protein

43
Q

What is the pathology of HD?

A

Stiratal GABAergic neurons (MSNs) die. This leads to a decreased striatal volume

44
Q

What is the role of the proteostasis network in HD?

A

The presence of inclusion bodies in neurons in HD suggest that there is a defect in the proteasome system, maybe it is overwhelmed with misfolded mHTT.

45
Q

What are the mechanisms for long-lasting changes in synaptic transmission during LTP?

A

Transcription Factors activated when phosphorylated by kinase increases transcription and gene expression leading to more AMPA receptors

46
Q

How does LTD occur in the hippocampus?

A

When the rate of Ca2+ ions coming into the cell decreases, phosphates are activated which decrease AMPA receptors on membrane

47
Q

What is Alzheimer’s disease?

A

AD is a progressive neurological disease of the brain with irreversible loss of neurons.

48
Q

What is the pathology of AD?

A

The pathology of AD shows extracellular beta-amyloid plaques and intracellular tangles of hyperphosphorylated tau in AD brains

49
Q

What are the beta-amyloid plaques composed of?

A

The plaques are composed of beta-amyloid peptide that are abnormally processed from a larger precursor APP protein

50
Q

What are neurofibrillary tangles?

A

Abnormally folded tau protein. In AD tau is hyperphosphorylated and form twisted strands. These tangles no longer bind to tubulin and therefore disrupt intracellular transport.

51
Q

How do plaques and tangles spread through the brain?

A

Plaques and tangles tend to spread through the cortex in a prion-like fashion.

52
Q

What are the early-onset genetic mutations that lead to AD?

A
  • APP is processed by secretases to make the beta-amyloid peptide. Mutations in APP lead to early-onset.
  • PSEN 1&2 are components of the gamma-secretase activity that cleaves APP
53
Q

What are the current drugs for AD? What do they do?

A

Memantine: NMDA receptor antagonist
NSAIDs: may alter where gamma-secretase cuts APP
Cholinesterase inhibitors: cholingeric neurons degenerate in AD

54
Q

What is poliomyelitis? How does it affect the body?

A

Neurotropic RNA virus that spreads via hand-mouth contact. Enters peripheral neurons via receptor and is transported to the spinal cord. Kills only LMN

55
Q

What is rabies? How does it affect the body?

A

Neurotropic RNA virus that enters salivary glands and causes froth. Transported along motor axons to the CNS

56
Q

What is HIV? How does it affect the body?

A

Human Immunodeficiency Virus causes AIDS. Retrovirus, that infects T-cells. Viral RNA transcribed into DNA inserted into host genome turning it into viral factory

57
Q

What is Botulism? How does it affect the body?

A

Bacterial toxin that causes flaccid paralysis by blocking ACh release

58
Q

What is Tetanus? How does it affect the body?

A

Bacterial toxin that affects motor neurons and causes spastic paralysis.

59
Q

What is the process of cellular nervous system development?

A

Position cells –> mitosis –> specify cell fates –> migration –> axonal growth –> synapse

60
Q

What are neurexins? Neuroligins?

A

Neurexins are presynaptic and localize synaptic vesicles and docking proteins. Neuroligins are postsynaptic and affect clustering of AMPA and NMDA receptors.

61
Q

What causes DS?

A

Due to an extra chromosome 21, a problem with gene dosage not with mutated proteins

62
Q

What is the enhanced GABAergic activity theory in DS?

A
  • Excessive GABAergic inhibition leads to increased LTD and decreased LTP.
  • GIRK2 = G-protein coupled K+ channel activated by GABA receptors
  • Olig 1 & Olig 2 = transcription factors that drive overgrowth of GABAergic interneurons
63
Q

What do you see in DS transgenic mice?

A

See decreased synapse density and decreased spine numbers but abnormally large spines and wrong placement of GABAergic synapses on the dendritic shaft instead of at the base of the spine head.

64
Q

What are treatments for DS? What are the risks?

A
  1. Blocking GABA-R
  2. GABA-A receptor antagonist
  3. blocking GIRK2
    * risky because blocking GABA can lead to seizures
65
Q

What causes Fragile X syndrome?

A

CGG expansion on X-chromosome (not on coding region- promoter region 5’ UTR) causes silencing of FMR1 gene

66
Q

What are the changes in spine morphology in FXS?

A

Increased numbers of long, thin dendritic spines

67
Q

How does enhanced mGluR5 signaling affect FXS?

A

Some mGluR5 regulated mRNAs are suppressed by fragile X mental retardation protein (FMRP) causing mGluR5 signaling to be exaggerated, leading to excessive LTD and abnormal spines

68
Q

What causes Rett Syndrome?

A

> 95% Rett syndrome is caused by de novo loss of function mutations in MeCP2 gene. MeCP2 can activate or inhibit gene expression.

69
Q

What dendritic spine changes do you see in Rett Syndrome?

A

Decrease in number and size

70
Q

What are the changes in synapses associated with Autism?

A

Increased synapses

71
Q

Parasympathetics have long _______ with ganglia near the _______ _______. Sympathetics have long _______ with ganglia near the ______ _____.

A

Parasympathetics have long pre-ganglionics with ganglia near the target organ.
Sympathetics have long post-ganglionics with ganglia near the spinal cord.

72
Q

What is the hypothalamic-pituitary-adrenal axis? (HPA)

A

The hypothalamus stimulates release of NT from the anterior pituitary which stimulates the adrenal cortex to produce glucocorticoids which activates the body’s stress response.

73
Q

What does lithium do in depression?

A

Lithium strengthens both pre- and post- synaptic activity of CA1 neurons. Pre-synaptically Li+ enhances BDNF release which enhances LTP and post-synaptically Li+ prolongs the opening of AMPA receptors

74
Q

Why is the HPA axis over-stimulated in stress?

A

Under normal conditions, the hippocampus exerts an inhibitory effects on the hypothalamus, but chronically elevated glucocorticoids and severe traumatic stress can cause hippocampal atrophy. Therefore this allows excessive hypothalamic activation of the HPA axis

75
Q

What are the treatments for depression?

A
  1. MAOI
  2. SSRIs
  3. Psychotherapy
  4. Ketamine
76
Q

What are the synaptic changes in schizophrenia?

A

Reduced synapse number due to developmental over-pruning in schizophrenia.

77
Q

What is the dopamine hypothesis for schizophrenia?

A

There is altered dopamine release from presynaptic terminals, but no change in D2 receptor number or transporters.

78
Q

What is the glutamate hypothesis of Schizophrenia?

A

Over-pruning of spines during development may cause glutamate hypofunction which leads to enhanced dopamine release.

79
Q

What is the GABA hypothesis in Schizophrenia?

A

Reduced GABA leads to an impaired E/I balance in DLPFC.

80
Q

What are the candidate genes for schizophrenia?

A
  1. DISC1
  2. COMT
  3. NRG-1
  4. Neuroligins & ErbB4
  5. Hemizygous deletion on c22q.11.2
81
Q

What are the treatments for schizophrenia?

A
  1. Anti-psychotic drugs are D2 antagonists
82
Q

What is angiogenesis in cancer?

A

Cancer cells secrete factors that stimulate the growth of blood vessels to feed the growing cancer cells

83
Q

What are the types of primary brain tumors?

A

Meningioma, Ependymoma, Medullaoblastoma, Gliomas = Astrocytomas, Glioblastomas, & Oligodendrogliomas

84
Q

What are the 4 features to look for when grading primary brain cancers?

A
  1. Pleomorphism = odd cells
  2. Mitosis
  3. Necrosis
  4. Neovascularization
85
Q

What is active migration?

A

Involves volume changes which are controlled by ion fluxes that affect osmosis.

86
Q

How do gliomas use excitotoxcity?

A

To grow a tumor, gliomas need a lot of space so they kill neurons via glutamate excitotoxcity. Glial tumor cells release glutamate via the cytesine/Glu exchanger.

87
Q

What is chlorotoxin?

A

A Cl- channel blocking peptide that binds to gliomas, by blocking Cl- movement, you can change osmosis so gliomas can’t change shape & move

Clinical Neuroscience (15 decks)

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