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EXP NEURO > Intro to Neurosci > Flashcards

Intro to Neurosci Flashcards

1
Q

list types of neuroscience: (5)

A
  • cognitive
  • behavioural
  • systems
  • cellular
  • molecular
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2
Q

define cognitive neuro:

A

understanding higher level (human) thought processing

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3
Q

define behavioural neuro:

A

biopsych, why/ how we produce certain behaviours

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4
Q

define systems neuro:

A

how brain controls body systems, how body systems provide info to brain

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5
Q

define cellular neuro:

A

how neurons/ glia work, signalling in cells

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6
Q

define molecular neuro:

A

how molecules/ chemicals work in brain cells to communicate, grow, change

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7
Q

animal welfare and ethics: proposal

A
  • proposal approved by Animal ethics committee under NHMRC (national health and medical research council)
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8
Q

animal welfare and ethics: use of animals

A
  • only for worthwhile new experiments to advance understanding
  • pain/ distress minimal
  • all possible alternatives considered
  • research follows Aus code for Responsible conduct of research
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9
Q

cognitive neurosci eg:

A
  • hippocampus, amygdala

- use of drugs trigger brain activity on PET, MRI

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10
Q

behavioural neurosci: list eg (3)

A
  • elevated plus maze (rats tested to see time spent in open/ closed arms)
  • anxiety
  • drug use
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11
Q

systems neurosci eg:

A
  • modify brain systems inject chemicals into certain brain areas
  • how it effects behaviour, BP, respiration etc.
  • done on freely moving/ anaesthetised animals
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12
Q

cellular neurosci eg:

A
  • immunohistochemistry (staining cell types)
  • electrophysiology
  • connectome
  • neural signalling w computer tech
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13
Q

molecular neurosci eg: (4)

A
  • proteomics
  • immunohistochem
  • neuroinflammatory markers
  • epigenetics
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14
Q

epigenetics: define

A
  • functional morphology: causal mechanisms which genes/ genotype bring phenotypic effects
  • molecular def: heritable changes in gene function not explained by changes in DNA sequence
  • molecular mechanisms that regulate and coordinate expression of genome
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15
Q

epigenetics: genome model interaction w env

A
  • og: env + genes –> influence behaviour

- now: env stimuli –> neuronal gene expression (incl epigenetic mechanisms) –> behaviour

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16
Q

epigenetics: why does it matter?

A
  • involved in 30+ human neurodev disorders
  • memory extinction involves epigenetic changes
  • Alzheimers
  • drug abuse, addiction
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17
Q

epigenetics: central concept of DNA

A

transcription - RNA processing - translation to become polypeptide

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18
Q

epigenetics: DNA comprises of

A
  • packaged around histone proteins
  • DNA + protein = chromatin
  • tightness influences accessibility of DNA sequence to transcription enzymes
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19
Q

epigenetics: DNA transcription

A
  • RNA polymerase unwinds helix, paired to RNA nucleotides
20
Q

epigenetics: pattern of gene expression will?

A
  • determines cell fate in dev, and ongoing cell function
21
Q

epigenetics: mechanisms- histone modification

A
  • changes how tight DNA sticks to histone proteins
22
Q

epigenetics: general method- DNA methylation

A
  • sticking methyl groups onto DNA chain
23
Q

histone modification: how histone + DNA bind

A
  • basic and +ve charged binding w acidic -ve DNA

- chemical mod change charge of histone

24
Q

histone modification: classes of mod (4)

A
  • acetylation
  • methylation
  • ubiquitinisation
  • phosphorylation
25
Q

histone modification: de/ACETYLation

A
  • add acetyl gorups to lysine aa within histone
  • neutralises +ve charge
  • exposes DNA
  • via histone acetyltransferases (HATs)
  • deacetylation: increase charge
  • via histone deacetylase (HDACs)
  • reduces likelihood of transcription
26
Q

histone modification: METHYLation HMT, HDM effects

A
  • add (HMT)
  • remove (HDM) methyl groups to lysine residues
  • depends may enhance/ silence transcription
27
Q

histone modification: METHYLation DNA ladder mechanism and effect

A
  • cytosine bases methylated = 5mC
  • DNMTs (DNA methyltransferase) add methyl to C/G in DNA
  • reduces transcription
  • maintenance DNMTs restore methyl groups after DNA replication
28
Q

histone modification: DNA METHYLation + deACETYLation how does it inhibit/reduce gene transcription? (*attraction)

A
  • physically interfere w binding RNA polymerase = inhibits transcription
  • methylated DNA attracts methyl DNA binding protein - adaptor protein - attract HDACs (histone deacetylase enzymes)
  • deacetylate histones increase binding histones to DNA
  • methylation usually reduces gene transcription (silences gene)
29
Q

histone modification: DNA de-METHYLation- Tet1 and DNMT effect summary

A
  • Tet1 (10-11 translocation methyl cytosine dioxygenase 1)
  • increase transcription
  • own stable epigenetic mark
  • DNMT reduces trans
  • focused on gene regulatory regions (promotor programming)
30
Q

neuroepigenetics:

A

epigenetic sys as regulators of neuronal function, influence output of neuronal circuits

31
Q

epigenetics: long term memory (LTM) hypothesis

A
  • LTM storage neurons must lock parameters so circuits stable output
  • epigenetic changes provide mechanism to lock stable patterns of gene expression = stabilise functional properties of cell
32
Q

Alzheimer’s disease: features

A
  • neurodegeneration (selective death of Ach cells)
  • slowly progressing dementia
  • memory loss
  • change in personality
33
Q

Alzheimer’s disease: apraxia

A

loss ability to coordinate movements

34
Q

Alzheimer’s disease: aphasia

A

loss ability to articulate ideas/ comprehend written/ spoken word

35
Q

Alzheimer’s disease: agnosia

A

can’t interpret sensory stimuli

36
Q

Alzheimer’s disease: protein and eg.

A
  • protein accumulation in/ around neurons
  • intracellular neurofibrillary tangles (NFT)
  • extracellular amyloid plaques (ß amyloid protein)
37
Q

Alzheimer’s disease: APP features

A
  • amyloid precursor protein
  • when cleaved (via secretases) to make secretory products in learning/ memory storage
  • OR ß amyloid plaques

= hypomethylation of APP in AD

38
Q

Alzheimer’s disease: tangles and plaques

A
  • amyloid plaques before NF tangles

- APP balance shifted (genetic, env?)

39
Q

Alzheimer’s disease: NFT features contd

A
  • abnormal cluster of hyperphosphorylated tau protein

- tau usually helps maintain axon shape, transport molecules from cell body –> terminals (microtubules)

40
Q

Alzheimer’s disease: genetic

A 
early onset (50s-60s) 15% is genetic
- hereditary mutations of APP processing (Aß42)

late onset (65-85yo)

  • apoE gene (predispose plaque deposits),
  • A2M (clears deposits, but mutates form doesn’t)
  • more dependant on env
41
Q

Alzheimer’s disease: list env factors (6)

A
  • nutrition (deficient Vit B, folate)
  • exposure metals, pesticides
  • stress
  • social factors (loss partner)
  • vascular risk factors (hypertension, diabetes)
  • brain trauma
42
Q

Alzheimer’s disease: chemical changes seen in post mortem brain (3)

A

multiple changes:

  • histone modification
  • DNA methylation state
  • causal vs consequential
43
Q

Alzheimer’s disease: mouse model

A
  • CDK5 (cyclin-dependant kinase-5) mouse
  • neuron loss ß Amyloid accumulation and Tau pathology, memory loss
  • increased HDAC2 at promoters vital for synaptic plasticity, memory (incl BDNF)
  • reduce HDAC2 expression reversed memory impairment
44
Q

Alzheimer’s disease: mostly product of

A
  • gene x env (epigenetic) interactions
45
Q

RNA polymerase: function (3)

A
  • id promotors of gene
  • signal where the gene starts
  • signal when to start transcription
46
Q

relo btw: 5-methylcytosine, 5-hydroxymethylcytosine, Tet1

A

Tet1: converts 5-methylcytosine into 5-hydroxymethylcytosine (5HmC)

  • promotes transcription
47
Q

ßamyloid for learning/ memory storage: % in normal vs AD

A
  • normal: 90%

- AD: 40%

EXP NEURO (10 decks)

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