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Neurobiology > Lectures 11+12 > Flashcards

Lectures 11+12 Flashcards

1
Q

axon degenerates when separated from cell body

A

Wallerian degeneration

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2
Q

changes in cell body

A

chromatolysis

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3
Q

How can peripheral neurons grow back after degeneration?

A

nerve “stump” or tract persists after axon degenerates –> peripheral axons grow back through this stump

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4
Q

Regenration is due to the ____. Occurs easily in __ but not the ___.

A

environment
PNS
CNS

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5
Q

Why is the environment in the PNS is hospitable to regeneration?

A
  • machrophages rapidly remove myelin debris
  • Schwann cells promote axon regeneration
  • axon growth-promoting signals
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6
Q

Why doesn’t regeneration occur in the CNS?

A
  1. components of myelin inhibit axon growth
  2. absence of growth-promoting substances
  3. astrocytes proliferate at site of injury and form glial scar tissue that blocks axon growth
  4. neuron itself has decreased ability to enter “growth state”
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7
Q

Cognitive decline with age varies among ___ and among ___.

A

individuals

tasks

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8
Q

What causes brain shrinkage with age?

A

decreased number of spines and therefore synapses (not decreased neurons!) –> synaptic de-differentiation?

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9
Q

___ in monkeys has shown to protect to an extent from age-related cognitive decline.

A

exercise and caloric restriction

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10
Q

progressive loss of structure and/or function of neurons

A

neurodegeneration

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11
Q

Neurodegeneration most commonly affects what?

A

movement and/or mental function

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12
Q

What are some characteristics of neurodegeneration?

A
  • incurable
  • many caused by genetic mutations
  • loss of neurons and synapses
  • accumulation of toxic intra- or extracellular proteins
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13
Q

a form of dementia (i.e., loss of brain function) that gradually gets worse over time and is caused by progressive neurodegeneration

A

Alzheimer’s

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14
Q

Alzheimer’s affects ___, ___, and ___. Early onset is often ___ and late onset is more common. Symptoms first appear as “____”

A 
memory
thinking
behavior
genetic
common
forgetfulness
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15
Q

hyperphosphorylated tau (microtubule- associated protein) found in Alzheimer’s neurons

A

tangles

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16
Q

clumps of beta-amyloid protein found outside of neurons in patients with Alzheimer’s

A

plaques

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17
Q

Amyloid deposition leads to what?

A

impaired learning and memory

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18
Q

Infusion of beta-amyloid into lateral ventricles leads to what?

A

impaired spatial memory

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19
Q

Where are beta-amyloid seen mostly?

A

in the hippocampus and regions of neurogenesis

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20
Q

In Alzheimer’s, there is a decrease in both ___ and ___ of neurons in the dentate gyrus. Neurogenesis is also inhibited in the ___.

A

SVZ

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21
Q

Studies have shown that in the first week after a stroke (ischemia), there is increased ____ of stem cell, even in areas outside of the ___.

A

proliferation

SVZ/SGZ

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22
Q

____ increase neurogenesis in adults. __ and ___ inhibit neurogenesis.

A

antidepressants
stress
depression

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23
Q

What are the current sources of neural stem cells?

A

embryonic - isolated from a blastocyst
somatic cells - induced pluripotent stem cells (skin cell)
adult - isolated from stem cell niches

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24
Q

What are some cell replacement strategies?

A

mobilizing endogenous NSC (antidepressants)

transplantation

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25
Q

layer of cells that surrounds blastocyst

A

trophoblast

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26
Q

hollow cavity inside blastocyst

A

blastocoel

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27
Q

~30 cells at one end of the blastocoel (stem cells)

A

inner cell mass

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28
Q

What are “embryo-safe” stem cells?

A

single-cell biopsy from blastomere (8- cell stage)  80% survival rate (consistent with non-biopsied embryos)

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29
Q

What are iPSCs?

A

induced pluripotent stem cells; “de-differentiate” cells whose developmental fates had been previously assumed to be determined

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30
Q

How do you de-deifferentiate a somatic cell?

A

genetically reprogram adult cells to an embryonic stem cell–like state by forced expression of stem cell-specific genes and factors

31
Q

What are the “4 magic genes” that need to be force expressed for de-differentiation?

A 
Sox2: self-renewal
Oct4: differentiation
switch
Klf4: p53 pathway, oncogene
c-Myc: global histone acetylation, oncogene
32
Q

What are some issues with ESCs?

A
  • ethical issues
  • difficult to access
  • immunologic rejection if transplanted
33
Q

What are some issues with iPSCs?

A
  • low efficiency

* virus + oncogenes

34
Q

What are some issues with adult stem cells?

A
  • not easily accessible
  • critical for normal neurological function
  • immunologic rejection if transplanted
35
Q

What is a potential source of autologous NSCs for transplantation?

A

filum terminale

36
Q

What are the advantages of the filum terminale?

A
  • expendable

* easily accessible

37
Q

What is the filum terminale?

A

vestigial remnant of spinal cord (i.e., no critical CNS function in adults)

38
Q

Why is selective or global degeneration (such as ALS or stroke) harder to treat with stem cells?

A

harder to establish the specific afferent-efferent and/or long-distance/local connections; more complicated than just replacing cells

39
Q

What are some issues with stem cells?

A
  • environmental cues: gliogenic cues overcome neurogenic cues
  • production of ectopic circuits
  • tumor formation
40
Q

Where are oxytocin and vasopressin hormones produced?

A

magnocellular cells of the hypothalamus

41
Q

What are the roles of oxytocin?

A
  • acts on uterus during childbirth
  • acts on mammary glands during lactation
  • promotes mother-infant bonding
42
Q

What are the roles of vasopressin?

A
  • acts on kidney to control salt balance and blood volume

* promotes social memory (previously encountered individuals)

43
Q

What happens when you inject a vasopressin antagonist in male prairie voles?

A

blocks pair bond formation (more like meadow voles)

44
Q

What happens when you inject an oxytocin antagonist in female prairie voles?

A

block pair bond formation (more like meadow voles)

45
Q

What happens when you express more vasopressin receptors in meadow voles?

A

enhance pair bond formation (more like prairie voles)

46
Q

What have studies shown about men with allele 334 of vasopressin receptor (“cheating gene”)?

A

• felt weaker bond with partner
• more likely to have had marital crisis
in past year
• wives were less satisfied with relationship

47
Q

What affect does oxytocin nasal spray have on humans?

A

unfamiliar faces perceived to be more trustworthy and more attractive by both males and females

48
Q

When is oxytocin released?

A
  • pair bonding and sex
  • mother-infant bonding
  • birth
  • lactation
49
Q

Children who experience neglect have long-lasting problems with ___
as well as lower ___ levels. In rats, higher levels of ____ lead to higher levels of oxytocin receptors in offspring, this persists into adulthood. Aka, early experience can have ___.

A

social bonding
vasopressin and oxytocin
maternal care
long-lasting effects

50
Q

disorder of social behavior; lack of social engagement; poor performance on tests like perceiving emotions on faces

A

autism

51
Q

What are some characteristics of autism?

A
  • inability to form emotional bonds with others (including parents)
  • impairment in communication skills, including spoken language
  • repetitive and stereotyped behaviors
52
Q

In one experiment, men with autism were less likely to recognize emotion and ___ improved this ability. It also boosted brain activity in ___. However, other studies have shown that ____ is not uniquely associated with disease.

A

oxytocin
amygdala and PFC
oxytocin

53
Q

distortion of thinking and perception

A

schizophrenia

54
Q

What are some symptoms of schizophrenia?

A
  • disorganized thoughts – “loose associations”
  • disorganized language – word salad, echolalia
  • delusions of influence, grandeur, or persecution
  • hallucinations
  • bizarre behavior
  • inappropriate or flat affect
  • lack of motivation
  • lack of insight
55
Q

What are the characteristics of schizophrenia?

A
  • late onset (teens, early 20s)

* psychotic episodes with “positive” symptoms alternate with periods of “negative symptoms” –> lifelong

56
Q

What is the dopamine hypothesis of schizophrenia?

A
  • hyperactivity of dopaminergic transmission responsible for schizophrenia
  • block D2 receptors - antipsychotic drugs
  • doesn’t explain negative symptoms
57
Q

What were the treatments for schizophrenia?

A

1) psychotherapy
2) electroshock
3) lobotomy
4) antipsychotic drugs

58
Q

What are the genetic influences for schizophrenia?

A

• high concordance (~50%) in
monozygotic twins
• 20% concordance in dizygotic twins (no more similar than other siblings)

59
Q

How do antipsychotic drugs work?

A

block dopamine receptors

60
Q

response to threat, absence of people/objects

that signify safety

A

anxiety

61
Q

Balance in favor of GABA (high) leads to what symptoms?

A

sedation, amnesia, ataxia

62
Q

Attenuation of GABA (low) leads to what?

A

arousal, anxiety, restlessness, insomnia

63
Q

What is used to treat anxiety disorders?

A

GABA agonists - increase inhibition

64
Q

recurrent and persistent thoughts, impulses, or images that are intrusive/unwanted and caused marked anxiety and distress

A

obsessions

65
Q

behaviors people perform to reduce/remove anxiety caused by obsessions

A

compulsions

66
Q

pervasive pattern of preoccupation with orderliness and perfectionism at the expense of flexibility and efficiency

A

OCD

67
Q

What are the characteristics of OCD?

A
  • preoccupation with details, rules, and lists so that the point of the activity is lost
  • perfectionism that interferes with task completion
68
Q

What is the serotonin hypothesis?

A

antidepressants that block serotonin uptake also have anti-obsessional activity –> low serotonin leads to OCD

69
Q

What is PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus)?

A

psychiatric symptoms such as OCD and tics (uncontrolled movements) in children causes by molecular mimicry from strep

70
Q

What affected areas seem to contribute to OCD?

A

orbitofrontal cortex, basal ganglia, striatum

71
Q

What happens during molecular mimicry?

A

cross reactivity of antibodies
produced against a group A streptococcal carbohydrate epitope, also recognize an antigen on the surface of neurons –> immune system recognizes self antigens as foreign

72
Q

How does PANDAS cause tics?

A

1) antibodies produced against surface protein of dopaminergic neurons –> cannot modulate dopamine release –> too much dopamine
2) antibodies produced against D2 receptor –> binding of antibodies causes a reduction of inhibitory effect
- -> more dopamine is released

**promote movement (e.g., tics)

73
Q

What can be used to treat PANDAS?

A

• cognitive behavioral therapy and/or anti-obsessive medications (e.g., SSRI)
• antibiotics to eliminate strep infection
• “blocking” antibodies to complex with antibodies
produced by your body
• prophylactic treatment to prevent future infections

Neurobiology (9 decks)

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