Intro to Neurosci Flashcards
1
Q
list types of neuroscience: (5)
A
- cognitive
- behavioural
- systems
- cellular
- molecular
2
Q
define cognitive neuro:
A
understanding higher level (human) thought processing
3
Q
define behavioural neuro:
A
biopsych, why/ how we produce certain behaviours
4
Q
define systems neuro:
A
how brain controls body systems, how body systems provide info to brain
5
Q
define cellular neuro:
A
how neurons/ glia work, signalling in cells
6
Q
define molecular neuro:
A
how molecules/ chemicals work in brain cells to communicate, grow, change
7
Q
animal welfare and ethics: proposal
A
- proposal approved by Animal ethics committee under NHMRC (national health and medical research council)
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
9
Q
cognitive neurosci eg:
A
- hippocampus, amygdala
- use of drugs trigger brain activity on PET, MRI
10
Q
behavioural neurosci: list eg (3)
A
- elevated plus maze (rats tested to see time spent in open/ closed arms)
- anxiety
- drug use
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
12
Q
cellular neurosci eg:
A
- immunohistochemistry (staining cell types)
- electrophysiology
- connectome
- neural signalling w computer tech
13
Q
molecular neurosci eg: (4)
A
- proteomics
- immunohistochem
- neuroinflammatory markers
- epigenetics
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
15
Q
epigenetics: genome model interaction w env
A
- og: env + genes –> influence behaviour
- now: env stimuli –> neuronal gene expression (incl epigenetic mechanisms) –> behaviour
16
Q
epigenetics: why does it matter?
A
- involved in 30+ human neurodev disorders
- memory extinction involves epigenetic changes
- Alzheimers
- drug abuse, addiction
17
Q
epigenetics: central concept of DNA
A
transcription - RNA processing - translation to become polypeptide
18
Q
epigenetics: DNA comprises of
A
- packaged around histone proteins
- DNA + protein = chromatin
- tightness influences accessibility of DNA sequence to transcription enzymes
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
histone modification: de/ACETYLation
- 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
histone modification: METHYLation HMT, HDM effects
- add (HMT)
- remove (HDM) methyl groups to lysine residues
- depends may enhance/ silence transcription
27
histone modification: METHYLation DNA ladder mechanism and effect
- 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
histone modification: DNA METHYLation + deACETYLation how does it inhibit/reduce gene transcription? (*attraction)
- 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
histone modification: DNA de-METHYLation- Tet1 and DNMT effect summary
- 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
neuroepigenetics:
epigenetic sys as regulators of neuronal function, influence output of neuronal circuits
31
epigenetics: long term memory (LTM) hypothesis
- 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
Alzheimer's disease: features
- neurodegeneration (selective death of Ach cells)
- slowly progressing dementia
- memory loss
- change in personality
33
Alzheimer's disease: apraxia
loss ability to coordinate movements
34
Alzheimer's disease: aphasia
loss ability to articulate ideas/ comprehend written/ spoken word
35
Alzheimer's disease: agnosia
can't interpret sensory stimuli
36
Alzheimer's disease: protein and eg.
- protein accumulation in/ around neurons
- intracellular neurofibrillary tangles (NFT)
- extracellular amyloid plaques (ß amyloid protein)
37
Alzheimer's disease: APP features
- 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
Alzheimer's disease: tangles and plaques
- amyloid plaques before NF tangles
| - APP balance shifted (genetic, env?)
39
Alzheimer's disease: NFT features contd
- abnormal cluster of hyperphosphorylated tau protein
| - tau usually helps maintain axon shape, transport molecules from cell body --> terminals (microtubules)
40
Alzheimer's disease: genetic
```
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
Alzheimer's disease: list env factors (6)
- nutrition (deficient Vit B, folate)
- exposure metals, pesticides
- stress
- social factors (loss partner)
- vascular risk factors (hypertension, diabetes)
- brain trauma
42
Alzheimer's disease: chemical changes seen in post mortem brain (3)
multiple changes:
- histone modification
- DNA methylation state
- causal vs consequential
43
Alzheimer's disease: mouse model
- 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
Alzheimer's disease: mostly product of
- gene x env (epigenetic) interactions
45
RNA polymerase: function (3)
- id promotors of gene
- signal where the gene starts
- signal when to start transcription
46
relo btw: 5-methylcytosine, 5-hydroxymethylcytosine, Tet1
Tet1: converts 5-methylcytosine into 5-hydroxymethylcytosine (5HmC)
- promotes transcription
47
ßamyloid for learning/ memory storage: % in normal vs AD
- normal: 90%
| - AD: 40%
