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Uni-year 1 & 2 > Brain and Behaviour > Flashcards

Brain and Behaviour Flashcards

1
Q

Basic brain facts

A

350g at birth, 1300g at adulthood
85 billion neurons, trillion of synapses
brain development and maturation not linear

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2
Q

what happens in germinal stage development

A
  • zygote formed - fusion of egg and sperm
  • through process of cleavage forms a cluster of homogeneous cells called morula
  • morula continues to divide-forms blastocyst
  • blastocyst implants in uterus
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3
Q

embryonic stage: gastrulation

A
  • embryonic disc
  • three distinct layers: ectoderm, mesoderm and endoderm
  • ectoderm folds within itself to form neural tube
  • neural tube becomes CNS
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4
Q

stages of brain development

A 
cell birth/proliferation
cell migration
cell differentiation and maturation
synaptogenesis and synaptic pruning
cell death
myelination
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5
Q

what happens at cell birth/proliferation

A
  • neurogenesis and gliogenesis
  • stem cells form progenitor cells
  • each progenitor cell can be neuroblast or glioblast
  • once formed, migrate out of ventricular zone
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6
Q

what is neurogenesis and gliogenesis

A

formation of new neurons

formation of non-neural glia

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7
Q

what is neuroblast and glioblast

A

cell that will form a neuron

cell that can form oligodendrocytes or astrocytes

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8
Q

what’s the alternative name for a progenitor cell

A

precursor cell

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9
Q

what happens in cell migration

A
  • cell movement to final destination
  • subventricular zone contains primitive map of cortex
  • predisposes cells born in specific regions to migrate to certain cortical zones
  • chemical signals and physical support aide cell migration
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10
Q

what are the chemical signals and physical support in cell migration

A

immunoglobins and cytokines

radial glia

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11
Q

what happens in differentiation and maturation stage of brain development

A
  • at destination, primitive neurons express particular genes
  • form axons and dendrites; give distinctive shape
  • differentiation dependent on destination
  • immature cells can acquire characteristics of location but once mature, lose that property
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12
Q

what occurs during dendritic development

A 
dendritic aborization (branching)
growth of dendritic spines
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13
Q

what happens during synaptogenesis and synaptic pruning stage

A
  • growth cone at end of axon develops extensions called filopodia
  • target sights release cell adhesion molecules and tropic molecules; attract growth cones
  • synaptic pruning: synapses activated maintained and strengthened, those not are eliminated
  • plasticity: ability to form and eliminate synapses
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14
Q

what happens at stage cell death

A
  • inactive synapses eliminated = neural darwinism
  • apoptosis= programmed cell death
  • survival signals are proteins secreted by target cells to promote survival and growth
  • neurotrophins and active communication prevents apoptosis
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15
Q

what happens in myelination stage

A
  • glia form fatty sheath surrounding axons
  • speeds transmission
  • first occurs in spinal cord, moves up towards forebrain
  • slow process
  • Schwann cells in PNS - singular cell surrounds singular axon
  • oligodendrocytes in CNS - singular cell surrounds multiple axons
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16
Q

research impact neurons

A
  • originally believed no new neurons form in adulthood
  • songbirds have steady replacement of neurons in ‘‘singing” region
  • olfactory bulb receptors continually replace dying ones
  • hippocampus neurogenesis to facilitate learning
  • cerebral cortex is controversial, following strokes or injury
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17
Q

regrowth of axons

A
  • better in younger brains or the periphery
  • destroyed body cells not regrow, but damaged axons can
  • collateral sprouting: new branches formed by non-damaged axons that attach to vacant spots on dendrites and cell bodies
  • secretion of neurotrophins allow collateral sprouting to occur
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18
Q

examples of brain adaptation

A
  • blind have enhanced tactile and auditory ability
  • burton 2002: braille letters, PET and fMRI showed activity of occipital cortex and increased response in visual areas of cortex due to auditory stimuli
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19
Q

critical periods of brain development

A
  • when brain most sensitive to experience
  • absence of visual stimuli lead to blindness or lack of exposure to language leads to ability to use it (blakemore and cooper-cats)
  • immature brain is vulnerable
  • chemical distortions in early development can cause sig impairment
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20
Q

neural tube defects

A
  • spina bifida: failure of closure of neural fold at level of spinal cord
  • anecephaly: brain fail to develop
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21
Q

impact of neglect and trauma on brain development

A
  • poor modulation of impulsivity - ‘primitive’ emotional and behavioural functioning
  • trauma environment lead to excessive active and reactive stress-response
  • overdevelopment of specific areas result in predisposition to aggression, impulsive and reactive behaviour
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22
Q

epigenetics

A

tracing disorders to development

environmental factors interact with genes

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23
Q

human dna facts

A

23 pairs chromosomes

share 99.9% dna wih eachother

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24
Q

dna structre

A

deoxyribonucleic acid
double helix of phosphate and deoxyribose
adenine, cytosine, guanine, thymine

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25
Q

what is the name for natural variations in DNA

A

single nucleotide polymorphisms (SNPs)

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26
Q

cell division

A

mitosis: somatic cells (genetically identical)
meiosis: gametes, homologous recombination (genetically different)

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27
Q

process of genes to proteins

A
  • transcription: transcription factor activated in development or intracellular signalling, gene DNA sequence copied to form mRNA
  • translation: ribosome attach to mRNA, reads triplet codons, tRNA forms amine acid chain
  • amino acid chain folds to form protein
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28
Q

Mendel’s law

A
  • inheritance through ‘transmissible units’

- Peas: height was dichotomous, small characteristic only visible in second gen

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29
Q

what are alleles

A

variants of gene
dominant or recessive
if identical called homozygous
if different called heterozygous

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30
Q

what is a genotype

A

genetic information

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31
Q

what is phenotype

A

physical appearance of genetic information

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32
Q

what is huntington’s chorea

A
  • single gene; autosomal dominant inheritance
  • degeneration of brain leads to progressive deterioration of movement, temperament and cognition
  • chromosome 4, excessive repeat of CAG bases
  • onset 35-55 years
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33
Q

what is phenylketonuria

A
  • single gene recessive inheritance
  • mutation in PAH gene (phenylalanine hydroxlase)
  • enzyme breaks down dietary phenylalanine
  • build in brain is toxic: epilepsy/learning disabilities
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34
Q

chromosomal abnormalities

A

monosomy: singel copy of chromosome
trisomy: three copies of chromosome

most are lethal

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35
Q

example of trisomy

A

downs syndrome
three copies of chromosome 21
smaller brain size, mild to mod intellectual ability and high risk of early Alzheimer onset

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36
Q

X-linked conditions

A
  • wrong number of chromosomes impact normal development
  • importance of gene dosage
  • Y chromsome mostly male sexual function genes
  • in activiation in females switches off one copy of X chromosome in embryogenesis
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37
Q

Rettsyndrome

A
  • progressive neurodevelopment disorder
  • almost exclusivet o females
  • profoudn mental impairment
  • mutation to gene MePC2
  • X in activation means not all cells express the mutated MePC2 gene
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38
Q

fragile X

A
  • most common inherited from of mental retardation
  • predominantly in male
  • mutation of FMR1 gene
  • amplification of CGG repeat
  • encodes for FMR protein
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39
Q

epigenetics

A
  • inherited change in phenotype
  • not due to change in genotype
  • environmentally activated
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40
Q

example of epigenetics

A

maternal care switches on seratonin, action through 5-HT7 receptor to activate transcription factor NGFIA whihc switches on gene for glucocorticoid receptor
absence of maternal licking: promoter methylated, low levels GR, increased stress hormones and anxiety/depression

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41
Q

gene association studies

A

sort SNPs in candidate gene
genome wide asosociation studies look for what SNPs associate with disease state
functional SNPs vs genetic tags

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42
Q

Alzheimer’s disease

A

mutation in genes
amyloid precurosor protien
risk genes identified using GWAS studies
one SNP difference between APOE3 and APOE4

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43
Q

polygenetic factors: twin studies

A

concordance rates

see how biological the inheritance is

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44
Q

genetics of schizphrenia

A

largely genetic but not purely

genes to do with synpatic transmission, glutamate and dopamine

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45
Q

what is voltage

A

difference in charge between two points

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46
Q

what is current

A

rate at which charge is flowing

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47
Q

structure of a neuron

A

dendrites
soma
axon
terminal boutons

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48
Q

resting potential

A
  • 65/-70mV
  • diffusion and electrostatic pressure of ions leads to equilibrium potential
  • sodium potassium pump ensures this it not met
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49
Q

what is equilibrium potential

A

force of diffusion = force of electrostatic pressure

initial conc important: high conc = large eq. pot.

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50
Q

Nernst equation

A

E = 61 x log(ion outside/ion inside)

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51
Q

where is action potential generated

A

axon hillock by summation of converging inputs from dendrites or electrical stimulation

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52
Q

what is hyperpolarisation

A

when membrane potential becomes more negative than resting pot.

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53
Q

what is depolarisation

A

when membrane pot. becomes more positive than resting pot.

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54
Q

what is the all or nothing principle

A

depolarisation must reach threshold for action potential to be generated, if it doesn’t there it not an action potential

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55
Q

stages of action potential

d = diffusion
ep = electrostatic pressure
A
  • resting pot. majority channels closed
  • small depolarisation opens a few sodium channels, d & ep into neuron
  • reach threshold, majority na channels open
  • as neuron depolarises, k channels open and k diffuses out
  • na channels refractory as positive potential reached, remaining k channels open
  • repolarisation - k diffuses out, membrane pot decreases
  • hyperpolarisation - some k channels close, na channels return to normal state
  • final k channels shut, membrane returns to resting pot due to na/k pump
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56
Q

propagation of action potential

A

unmyelinated: depolarisation along whole length of axon
myelinated: depolarisation only at nodes of ranvier

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57
Q

multiple sclerosis

A

damage to myelin sheath

results in loss of sensitivity, muscle weakness, difficulty with coordination and balance

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58
Q

types of synapse

A

electrical: rare in adult mammalian neurones, gap spanned by proteins which communicate between neurons
chemical: neurotransmitters

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59
Q

types of synapse location

A

axodendritic: dendrite to dendrite
axosomatic: dendrite to cell body
axoaxonic: dendrite to dendrite of another neuron to the cell body of another neuron

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60
Q

why is location of synapse important?

A
  • activation of excitatory synapse = local and small depolarisation (EPSP)
  • decays over length of dendrite
  • closer to soma the greater influence on production of action potential in axon
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61
Q

process at a chemical synapse

A
  • action pot arrive at terminal button
  • depolarisation opens voltage gated calcium channels
  • calcium diffuses in
  • vesicles containing neurotransmitter fuse with membrane and release into gap
  • binds to receptors on postsynaptic cell
  • depolarisation or hyperpolarisation
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62
Q

classes of neurotransmitter

A 
amino acids
monoamines
soluble gases
acetylcholine
neuropeptide
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63
Q

ionotropic receptors

A

ion channels

excitatory or inhibitory

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64
Q

metabotropic receptor

A

g protein coupled receptor

  • neurotransmitter bind to receptor and activate g protein
  • g protein splits and activates otehr enzymes
  • break down of GTP turns off g protein activity
  • series of chemical reactions lead to amplification of signal (secondary messenger)
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65
Q

what is glutamate

A

excitatory neurotransmitter in CNS

activates different types of receptors eg AMPA receptors

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66
Q

what is GABA

A

inhibitory neurotransmitter
activates ionotropic receptor which opens chloride channels
-involved in anxiety
-certain hormones or drugs enhance its activity

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67
Q

autoreceptors

A

located on presynaptic terminal
regulate internal process controlling synthesis and release of neurotransmitter
neg feedback system

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68
Q

categories of neurotransmitter

A

classical: amino acids, monoamines, acetylcholine

neuropeptides

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69
Q

synthesis, storage and break down of glutamate

A
  • synthesised in nerve terminal from glucose or glutamine
  • stored in vesicles by vesicular glutamate transporters
  • released by exocytosis
  • reuptake by excitatory amino acid transporters
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70
Q

what happens if amino acid transmitter release is not regulated

A

hyperexcitability - epilepsy

excitotoxicity

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71
Q

action of neurotransmitters at receptors

A

agonist: produces a cellular reaction
antagonist: blocks activity or agonist or ligand

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72
Q

what is kinetics, selectivity and conductance

A

rate of transmitter binding and channel gating determine duration of effects

what ions are fluxed

rate in flux

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73
Q

glutamate receptor diversity

A

three ionotropic receptors

  • NMDA
  • AMPA
  • Kainate
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74
Q

what are the agonist and antagonist of NMDA receptor

A

agonsit: NDMA/glutamate
antagonist: APV

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75
Q

what are the agonist and antagonist of AMPA receptor

A

agonist: AMPA/glutamate
antagonist: CNQX

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76
Q

what are the agonist and antagonist of kainate receptor

A

agonist: kainic acid/glutamate
antagonist: CNQX

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77
Q

how does NMDA receptor work

A

at resting: binding of glutamate opens the channel but nothing passes through as mg2+ s blocking the pore
depolarised membrane pushes out the mg2+, so the channel is open and ions can move

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78
Q

selectivity and conductance of AMPA/kainate and NMDA receptors

A

AMPA: fast opening channels and permeable to na/k

NMDA: slow opening, permeable to ca, na, k and requires glycine

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79
Q

dysregulation of NMDA receptors

A
  • receptor blocked by phencyclidine and MK801, produces symptoms that resemble hallucinations associated with schizo
  • glutamate excitotoxicity caused by excessive ca influx, activates calcium dependent proteases and phosholipases that damage cell
80
Q

GABA synthesis, storage, reuptake

A
  • synthesised from glutamate
  • stored in vesicles by vesicular GABA transporter
  • released by exocytosis
  • reuptake by transporters on glia and neurons including non-GABAergic neurons
81
Q

what happens if amount of GABA isnt regulated

A

too much = coma/sedation
-GHB gamma hydroxybutyrate is a GABA metabolite that cna be converted to GABA, moderate dose gives effects of alcohol, too much leads to unconsciousness

82
Q

GABA receptor diversity

A

GABA iontopic receptors: ligand gated channels with fast IPSP

GABA metabotropic receptors: G protein coupled, indrectly coupled with K or Ca through 2nd messenger, slow IPSP

83
Q

GABA a receptor

A

heteropentameric structure

  • 2 alpha, 3 subunits
  • Cl channel gated by binding of GABA
  • complex receptor with multiple binding sites
  • agonist: muscimol
  • non competitive: benzo, barbs
84
Q

evidence of GABAergic dysfunction in anxiety disorders

A
  • PET radiolabelled flumazenil
  • panic disorder patients fewer benzo bindign sites
  • lack sufficient inhibitory control in cortical and limbic regions to suppress inappropriate fear responses
85
Q

problems with barbiturates

A

general depression of neuronal activity: including vital functions
poor therapeutic ratio
dependency and withdrawal
only for severe insomnia

86
Q

advantage and disadvantage of benzodiazepine

A
  • fast acting anxiolytic
  • large therapeutic window
  • may cause dependence
  • effects potentiated by alcohol
87
Q

diffuse modulatory systems

A

specific populations of neurons that project diffusely and modulate activity of glutamate and GABA neurons in target areas

88
Q

what is neuromodulation

A

altering of presynaptics cells ability to release more transmitter or postsynpatic cells ability to respond

89
Q

what systems is dopamine involved in

A

midbrain projects to forebrain

  • nigrostriatal : movement
  • mesolimbic: reinforcement and reward
  • mesocortical: memory and planning
90
Q

synthesis, storage and reuptake of dopamine

A
  • synthesised from tyrosine by tyrosine hydroxylase to form L-DOPA which is synthesised by dopa decarboxylase to form dopamine
  • loaded into vesicles
  • reuptake by transporters powered by electrochemical gradient, enzymatically regarded by monoamine oxidases
91
Q

regulation of tyrosine hydroxylase activity

A

feedback inhibition by end products: dopamine competes for binding with essential factor

  • presynaptic activity lead to phosphorylation of TH which increases its activity
  • prolonged activity in presynaptic neuron leads to increase in transcription of TH gene leading to more enzyme synthesised
92
Q

drugs affecting dopamine synthesis and storage

A

reserpine impairs storage of monoamines
AMPT inactivates TH
psychostimulants like cocaine block reuptake of monoamines

93
Q

noradrenergic system

A

role in arousal and attention

dysfunction: anxiety, depression, heroin withdrawal

94
Q

seratonergic system

A

raphe nuclei with diffuse projections
descending projections to cerebellum and spinal cord
function in: mood, sleep, pain, emotion, appetite

95
Q

serotonin synthesis, storage and reuptake

A

tryptophan synthesised by tryptophan hydroxylase, forms 5-HCT which is catalysed by aromatic amino acid decarboxylase

  • loaded into vesicels
  • reuptake by transporters and degraded by MAOs in cytoplasm
96
Q

drugs affecting serotonin release and reuptake

A
  • fluoxetine blocks reuptake
  • fenfluramine causes release of serotonin and inhibits uptake
  • MDMA causes noradrenaline and serotonin transporters to run in reverse
97
Q

cholinergic system

A

acetylcholine

basal forebrain complex

98
Q

synthesis, storage and reuptake of acetylcholine

A

made from choline
loaded in vesicles
released dependent on calcium exocytosis
rapidly degraded in synaptic cleft by acetylcholinesterase

99
Q

drugs affects acetylcholine release and reuptake

A

acetylcholinesterase inhibitors block breakdown of Ach

botulinum and tetanux toxins block docking of vesicles

100
Q

disorders related to cholinergic system dysfunction

A

peripheral: myasthenia gravis
brain: alzheimer
addition
epilespy

101
Q

what is learning

A

response of brin to environmental events and involves adaptive changes in synaptic connectivity which results in behavioural changes
strengthening and weakening of synapses

102
Q

what is long term potentiation

A

mechanism underlying synaptic strengthening

results in long lasting increased synaptic efficacy

103
Q

properties of long term potentiation

A

temporal: summation of inputs reaches threshold that leads to induction of LTP
input specific: LTP at one synapse is not propagated to adjacent synapse
associative: simultaneous stimulation of strong and weak pathway will induce LTP at both pathways

104
Q

molecular mechanism of LTP

A

glutamate released onto inactive cell
AMPA receptor activated creating EPSP
NMDA receptor blocked by mg
depolarisation by MAPA not sufficient to unblock NMDA receptor
Glutamate released onto active cell
NMDA unblocked
Ca entry activated calcium calmodulin dependent protein kinase II
CaMKII phosphorylates AMPA receptors increasing effectiveness and stimulates insertion of new AMPA receptors into post synaptic membrane

105
Q

Ca calmodulin-dependent protein kinase

A

sustains activity after repolarisation
autocatalytic activity: phosphorylates self, no longer requires Ca
molecular switch maintains increased excitability of neuron

106
Q

presynaptic events in LTP

A
  • post synaptic neuron feed back to presynaptic by retrograde neurotransmitter (Nitric oxide)
  • Ca diffuse through NMDA and activates nitric oxide synthase
  • NO diffuses from site of production and activates guanylyl cyclase in presynaptic
  • guanylyl cyclase produces secondary messenger cGMP
  • signal transduction cascade lead to increased glutamate release from presynaptic bouton
107
Q

late phase LTP

A

protein synthesis required
protein synthesis inhibitors prevent consolidation of term term memories and LTP
stages of memory formation: acquisition, consolidation and recall

108
Q

early vs late phase LTP

A

early: lasts minute to hour, explained by movement of Ca and enhancement of AMPA receptors
late: hours, days months, requires Ca activated signal transduction cascade to activate new protein synthesis

109
Q

long term depressin

A

created in slice preparations by high frequency stimulation

AMPA receptors are dephosphorylated and removed from membrane

110
Q

Theta rhythms

A

hippocampal theta activity accompanies behaviours such as running, swimming and spatial orientated responses in rats
seem play role in synchronising activity id different brain regions

111
Q

manipulating LTP

A

genetically: increased amounts of particular NMDA receptor enhances LTP
age: as get older, decreased LTP as decreased expression NMDA receptors
enrichment: more enrich environment, potentiate LTP

112
Q

fear and anxiety disorders

A

fear is useful and innate response

anxiety disorders are by-product of inappropriate fear responses

113
Q

amygdala and fear

A
  • Kluver-Bucy syndrome: disorder when both right and left medial temporal lobes malfunction, little or no fear response
  • Feinstein 2011: women with bilateral amygdala lesions had little fear responses to films
114
Q

fear elicits the stress response, what are the steps that occur

A
  • sensory info to amygdala
  • amygdala excites locus coeruleus and hypothalamus
  • hypothalamus releases CRH
  • Pituitary response releases ACTH
  • Adrenal cortex releases cortisol
  • Locus coeruleus releases noradrenaline
115
Q

what does the sympathetic nervous system and CNS do when fight or flight response activated

A

sym: increases HR & BP, blood flow to muscles, fast breathing, perspiration and inhibited digestion
CNS: behavioural arrest & arousal, narrowing of attention, augmented startle response, cortical activation and emotional response

116
Q

Role of GABAergic receptors in anxiety disorders

A

PET study with radiolabelled flumazenil
panic disorder patients have fewer benzodiazepine binding sites
frontal cortex hyperactive responsiveness during periods of anxiety

117
Q

effects of benzodiazepine

A 
anxiolytic
anticonvulsant
sedative
muscle relaxant
amnestic
-partial agonist best therapeutic ratio
118
Q

animal models for anxiety

A

elevated maze: anxiety is degree to which avoids open arms of maze, diazepam increases time spent in aversive open arms

119
Q

genetically turning of BZD binding site

A
  • 5 subunits form doughnut structure around ion channel
  • BZD binding is dependent on histidine on N-terminal in extracellular domain
  • ‘knock in’ mice made with insensitive BZD subunit
120
Q

BZD and amygdala

A
  • high density of BZD bidning sites in amygdala
  • injection of soluble BZD into amygdala induces anxiolytic effect in rats
  • injection of BZD antagonist abolishes anxiolytic effect of BZD given systematically
  • even after amygdala destruction, BZD retains anxiolytic effect
121
Q

hippocampus and anxiety

A
  • provides info about contextual stimuli important for fear conditioning
  • lesions have anxiolytic effect
  • BZD direct effect on GABAergic inhibition in hippo
  • chronic stress; chronic activation of glucocorticoid receptors in hippo, excitotoxic
122
Q

locus coeruleus and anxiety

A
  • events important for survival lead to firing of LC
  • noradrenergic projections to cerebellum, hippo, neocortex and thalamus
  • increased arousal and attention
  • BZD decreases noradrenergic release
123
Q

raphe nucleus and BZD

A
  • Serotonergic projections to striatum, nucleus accumbens, frontal cortex and hippocampus
  • Punishment stimuli -> activation of serotonergic system -> behavioural inhibition
  • BZD decrease serotonergic activity in RA
124
Q

definition of schizophrenia

A

‘break from reality’

split mind

125
Q

positive symptoms of schizophrenia

A

thought disorders: disorganised, irrational, rhyming

delusions: persecution, grandeur, control
hallucinations: auditory an olfactory

126
Q

negative symptoms of schizo

A 
flattened emotional response
poverty speech
lack initiative
persistence
anhedonia
social withdrawal
127
Q

cognitive symptoms of schizo

A 
difficulty sustaining attention
low psychomotor speed
deficits in learning an dmemory
poor abstract thinking
poor problemsolving
128
Q

schizo performance on stroop and wisconsin card tests

A

schizo are slower and less accurate at stroop

schizo don’t show same increase in regional blood flow to dIPFC

129
Q

sensory-motor gating deficits in schizo

A

difficulty screening our irrelevant stimuli and focusing on salient one

  • p50 signal, schizo show no change in response to second auditory stimulus
  • pre pulse inhibition: schizo do not show startle response inhibition
130
Q

oculomotor functions of schizo

A

eye movement in tracking a moving stimulus is not smooth compared to control

131
Q

structural differences of schizo brain

A

size of lateral ventricles is twice as big as normal person

reduced brain volume in temporal, frontal lobes and hippocampus

132
Q

heritability of schizo

A

-adoption and twin studies show heritable trait but not due to one single gene
mutation of DISC1 gene: increases chances of schizo
paternal age: older fathers more likely schizo child
-monochorionic MZ twins 60% concordance

133
Q

early neurodevelopmental model of schizo

A

events in early life casuedeviations from normal development
-lie dormant until brain matures sufficiently enough to activate affected systems
early events such as infections, obstetric complications, nutritional deficiencies

134
Q

evidence of early neurodevelopmental mdoel of schizo

A

walker 1994: hoem movies, children displaying more negative affect and abnormal behaviour had schizo
schiffmann 2004: less sociability and deficient psychomotor functioning develop schizo

135
Q

late neurodevelopmental model of schizo

A

schizo results from abnormality or deviation in adolescence when synaptic pruning takes place

136
Q

two hit model of schizo

A

atypical development in early brain development and adolescence

  • early-dysfunction of specific neural networks that account for premorbid signs
  • adolescence-excessive synaptic pruning and loss of plasticity may account for emergence of symptoms
137
Q

dopamine hypothesis of schizo

A
  • abnormalities in DA functioning in brain
  • overactivity of DA in mesolimbic system result in positive symptoms
  • underactivity of DA in mesocortical results in neg and cog symptoms
138
Q

evidence of DA hypothesis of schizo

A

DA agonist induces psychosis

symptoms alleviated using antipsychotics which are antagonists

139
Q

problems with DA hypothesis

A

only explains part of schizo

140
Q

glutamate hypothesis

A

hypofunction of NMDA receptors

141
Q

evidence of glutamate hypothesis

A

phencyclidine and ketamine cause positive negative and cog symptoms
both are NMDA antagonists
glutamate agonsit improves pos and neg symptoms

142
Q

neuroinflammatroy hypothesis of schizo

A

microglial activation
brains immune cells hyperactive in people at risk of schizo
animal studies show link between pro-inflammatory agens and schizo symptoms
symptoms reversed with antibiotic aimed at microglial

143
Q

oestrogen hypothesis of schizo

A

estrogen plays protective role
peak onset of schizo around menopause
women less severe symptoms, later onset, better response to treatments

144
Q

antipsychotics

A

2 major families: D1 and D2
both both D2 receptors
20-30% people not respond
long term treatment leads to symptoms resembling parkinsons or tardive dyskinesia: unable stop moving

145
Q

atypical antipsychotics

A

for those resilient to the others
no parkinson effects
improves both pos and neg symptoms
clozapine: reduces suicide rates

146
Q

definition of sleep

A

natural, periodic state involving reduced response to environmental stimuli and decreased mobility

147
Q

what are the two processes that control sleep

A

homeostatic - accumulate sleep debt if not get enough

circadian - happens at particular time in 24hr cycle

148
Q

what is actigraphy

A

use of special watches to record activity during day and night

149
Q

what is polysomnography

A

recording of electrical activity from multiple sources
EEG - brain/neurons
EOG - eye movement
EMG - muscles

150
Q

what waves present when awake

A

beta - irregular, 13-30Hz

alpha - 8-12Hz, when resting

151
Q

stages of sleep

A

1-theta activity (transition)
2-sleep begins, irregular activity, spindles and k complexes
3-high amp low freq delta activity, regular and synchronised, body functions slow
REM - increased brain activity, asynchrony, facial twitches, erections etc

152
Q

what is sleep cycle and how long last

A

when fall asleep progress through 1-3, then cycle back through 1-3 then enter REM
each cycle lasts 90mins

153
Q

contemporary views on dreaming

A

activation synthesis hypothesis:
-brainstem activated during REM, send signal to cortex, creates images from memory, less activation of frontal cortex so no logic of timing
coping hypothesis:
-dream about events find threatening

154
Q

neural basis of sleep

A

melatonin secreted by pineal glands during dark promotes sleepiness
adenosine accumulates during day after prolonged wakefulness and promotes sleep

155
Q

brain inhibition during sleep

A

constantine: patients with encephalitis have continuous sleep and only wake for food drink etc, damage to base of brain
vIPOA: contains GABA, damage to vIPOA causes insomnia in rats, electrical stimulation causes sleepiness

156
Q

brain mechanisms of wakefulness (moruzi and mogoun 1949)

A

when anesthetised cats brainstem was stimulated, brain waves changed from delta to beta waves, the cats then woke up

157
Q

role of orexin/hypocretin

A

peptide released from lateral hypothalamus
highly responsible for maintenance of wakefulness
implicated in narcolepsy

158
Q

what is a circadian rhythm

A

rhythms or regular patterns of activity associated with 24 hr cycle
humans are diurnal

159
Q

early discoveries of biorhythms

A

not unique to humans and animals
mimosa plant continues rhythmic behaviour even when removed from light and temp
humans in underground bunker with no cues, maintained daily rhythms but it shifted to 25hrs

160
Q

setting and resetting the biological clock

A

zeitgebers are external cues, when resets biorhythm the rhythm is entrained
most potent zeitgeber is light

161
Q

jet lag and circadian rhythms

A

disruption of circadian rhythms due to crossing time zones
stems from mismatch of internal cloc and external time
phase delay - travelling west
phase advance - travelling east

162
Q

variability of circadian rhythms

A

-chronotypes - larks and owls
rhythms have genetic basis but change as function of age
children and elderly are larks, in adolescence tend to ward larks

163
Q

experiment that detected biological clcok

A

richter
electrical lesions of rat brain regions
lost rhythmic behaviour when lesion hypothalamus

164
Q

suprachiasmatic nucleus

A

in hypothalamus, lies above optic chasm
if lesioned, still engage in rhythmic behaviours, just haphazardly
single cell extracted continues rhythmic firing

165
Q

how does light reach SCN

A
  • receives info from retinohypothalamic tract

- made of photosensitive retinal ganglion cells with pigment called melanopsin which can respond directly to light

166
Q

how does SCN work

A

hall and rosbach 1984 - PER protein builds up in cells overnight and is broken down during day
young 94 - TIM protein meets PER, combine and shut down period gene

167
Q

feedback loop of SCN

A

transcription from DNA to mRNA, to translation to proteins which form dimers
dimers enter nucleus and inhibit transcription
dimers decay
cycle begins again

168
Q

other effects of scn

A

breeding: control of pineal gland, increased melatonin inhibits gonads, in summer less melatonin, gonads enlarge, produce testosterone
time of day affects performance on cog tasks

169
Q

why do we sleep

A

sleep is ubiquitous

  • adaptive: conserve energy
  • restorative: feel refreshed, remove free radicals from brain
  • learning and memory: REM enhance non-declarative tasks, slow wave enhance declarative tasks
  • developmental: brain development in babies
170
Q

sleep epidemic

A

modern societies getting busier
compromise sleep for activities chronically sleep deprived if 6hr or less every night
insufficient sleep -> mood disorders

171
Q

what is a somatosensory system

A

a system al over the body that allows us to distinguish between what world does to us and what we do
bodily sensations such as touch, temp, pain, position/movement

172
Q

what are nocioreceptors

A

free nerve endings
perception of pain and temperature
damage to dendrite or surrounding cells releases chemicals that stimulate dendrite and produces action potential

173
Q

what are haptic receptors

A

dendrite attached to hair, connective tissue
distinguished touch, pull, vibration, indention, flutter
mechanical stimulation produce action pot.

174
Q

what are proprioceptors

A

perception of location and body movement

movements stretch receptors to mechanically stimulate dendrite and produce action potential

175
Q

sensory receptor adaptation

A

slow adapting : signals presence of long sustained stimulus

rapid adapting: respond at beginning and end of stimulus

176
Q

dorsal-root ganglion neurons

A

carry info from skin to CNS via spinal cord
each spinal cord segment has one d-r gn each side
in spinal cord, axons may synapse onto other neurons or continue up to brain

177
Q

what is deafferentiation

A

loss of incoming sensory input due to damage of sensory fibres

178
Q

what is the dorsal spinothalamic tract

A

carry haptic and proprioceptive info

  • axons from d-r gn enter spinal cord
  • ascend ipsilaterally until synapse in dorsal column nuclei
  • axons from column cross over to opposite side and brain and project up through brainstem as part of medial meniscus pathway
  • axons synapse with neurons in ventrolateral nucleus of thalamus, projects to somatosensory cortex and motor cortex
179
Q

ventral spinothalamic tract

A

nocioreceptive info

  • axons from d-r gn enter spinal cord and cross over
  • synapse onto contralateral side
  • ascend to brain where join with other axons forming medial lemniscus
  • synapse with neurons located in ventrolateral nucleus of thalamus
  • project to somatosensory cortex
180
Q

monosynaptic reflex

A

relfex requiring one synapse between sensory input and movement

181
Q

what is the vestibular system

A

receptors in each inner ear that respond to body position and movement of head
three semicircular canals and otolith organs

182
Q

how does vestibular system work - semicircular canals

A

fluid in semicircular canals pushes against hair cells, causing bending of cilia, responds to angular acceleration, lead to potentials in cells
-direction of cilia bent determines if hair cell is depolarised or hyperpolarised

183
Q

how does vestibular system work - utricle and saccule

A

gelatin and octonia push against hair cells, altering rate of action potentials of cells that form vestibular nerve
respond to linear acceleration

184
Q

hierarchal organisation of homunculus

A

areas 3a and b project to area 1, whihc projects to area 2

each successive relay of info, increases size of receptive field

185
Q

forebrain role in movement

A

prefrontal cortex: planning of movement, specify goal
premotor cortex: organise motor sequence
primary motor cortex: produce specific skilled movements

186
Q

topographic organisation

A

neural spatial representation of body

parts of motor cortex that controls hands, fingers and lips and tongue are larger

187
Q

corticospinal tracts

A

bundle of nerve fibres directly connecting cerebral cortex to spinal cord
originates from layer V pyramidal neurons
branches at brainstem
lateral tract : opposite side of body, move digits and limbs
ventral tract: same side body, moves muscles of midline body

188
Q

motor neurons

A

project to muscles of body
laterally located neurons project to muscles that control fingers and hands
intermedially project to shoulders and arms
most medially project to msucles that control trunk

189
Q

extensor and flexor muscles

A

e-move limb away from trunk

f-move limb toward trunk

190
Q

characteristics of motor cortex neurons

A

planning and initiating movements
code force of movements
simple coding of mvoement direction

191
Q

volume hypothesis

A

internal globus pallidus acts like volume dial and projects to thalamus which projects to motor cortex

direct: inhibitory effect of GPi as too muhc activity lead to overactivity in thalamus, amplifies force of movement
indrect: excitatory effect on GPi too muhc activity lead to underactivity in thalamus and reduced force movement

192
Q

what is huntingtons chorea

A

muscle coordination affected
abrupt, excessive spontaneous irregularly timed movements
atrophy og caudate nucleus an dputamen
antipsychotics or anxiolytic drugs

193
Q

what is hemiballism

A

caused by stroke to subthalamic nucleus
results in involuntary fast movements
dopamine blocker

194
Q

what is parkinsons disease

A

affects movement, muscel control and balance
loss of sub nigra that sends dopamine projections to putamen
L-dopa

195
Q

mouse model of PD

A

symptoms induced following dopamine projection lesions in striatum
light sensitive D1R-expressing neurons in lesioned area
optogenic activation of D1R-expressing striatal neurons by shining blue light onto striatum
improvement in fine movement

196
Q

cerebellum and movement

A

acquiring motor skill
flocculus: small and dense lobe involved in eye movement and balance
lateral hemisphere: controls movement of limbs, hands, feet and digits
medial hemispheres: controls movement of face and midline body

197
Q

what ae the main motor functions of cerebellum

A
  • timing of movements
  • maintaining movement accuracy
  • motor associative learning

Uni-year 1 & 2 (12 decks)

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