Behavioural and Cognitive Neuroscience (UA_2015FBDBMW)
Institution
Universiteit Antwerpen (UA)
In this summary (based on my own notes and PPT) you can find all the chapters that are given in the Behavioral and Cognitive Neuroscience, except that last chapter about the cerebellum.
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-Dark pink = 1.1.
-Light pink = 1.1.1.
-Green= 1.1.1.1
- Blue= 1.1.1.1.1
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Behavioural and Cognitive Neuroscience (UA_2015FBDBMW)
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PERSONALITY BEHAVIORAL & COGNITIVE NEUROSCIENCE:
PERSONALITY NOVELTY SEEKING ADDICTION
temperament + character
III. SYSTEMS OR HIERARCHICAL APPROACH > twin & family studies
= predisposed how to = disposition (some- = PS has 3 layers: > neuropharmacology studies
react in situations thing acquired) in > persona = external layers = mask for > neurobehavioral studies of learning
→ basis for basic individual ≠ in values ≠ occasions > psychometric studies
emotions: eg. & goals → change behavior based on persons PERSONALITY = UNIQUE
anger & disgust → develops during or situations based on this all he developed the first tool
→ hardwired from life bcs of > the self = ego behind mask = tridimensional personality questionnaire COMBINATION OF
birth experiences → dominates conscious experience UNIVERSAL BUILDING
→ closely related personal TPQ BLOCKS
throughout history many philosophers & memories scale based on 3 dimensions/personality Cloninger convinced genetics !!!! +
researchers tried to distinguish personality > the unconscious awareness = not traits: determines how you react -> bcs everyone
groups normally accessible to conscious > novelty seeking traits genetically in- reacts ≠
→ always 4 big categories: awareness > harm avoidance dependent & determined → genetic variance ~ Gaussian distribut.
eg. Hippocrates: based on bodily fluids > reward dependence by specific B mechanisms → most people intermediate values
eg. Keirsey’s 4 temperaments REVIVAL TRAIT THEORY → at both ends extreme variants
→ used for personality all studies distinguish 5 main aspects that • each dimensions 4 subdivisions → = personality disorders
questionnaire & coupled to distinguish ≠ people • self-report: 15min
success = the big 5 • 100 T/F questions: eg. I am much + P also influence by sex:
more controlled than most people > HA & RD: ♀>♂
DEFINITION I. EXTRAVERSION: energetic people -> show → RD also influenced by age & cultural
Allport (psychologist) has 3 approaches: positive emotions, surgency (quick in factors
I. OMNIBUS DEFINITION: personality (PS) = thought & reactions), simulation seeking → eg. in Japan = job = life -> will
everything that makes you an individual II. AGREEABLENESS: more compassionate & determine a lot of things
→ it’s the integration & interaction of care about others > NS & PS: ♀ = ♂
genetic inheritance, experience & III. CONSCIENTIOUSNESS: self-discipline,
ways to relate the 2 act dutifully & aim for achievement TPI TCI TEMPERAMENT CUBE
→ okay to describe personality, but IV. NEUROTICISM: go more to negative = 7 PS scale:
not to discriminate personalities side of feelings = representation how ≠ PS-aspects work
> 4 ~ temperament: novelty seeking, together to form persons PS
II. TRAIT OR INTEGRATIVE / V. OPENNESS: more open to new things: art, harm avoidance, reward dependence
CONFIGURATIONAL APPROACH: trait emotion, adventures,... → combo’s of building blocks describe
& persistence
= dynamic trend of behavior which way of behaving & reacting
> 3 ~ character: self-directedness,
results from integration of numerous PSYCHOBIOLOGICAL MODEL OF cooperativeness & self-transcendence
→ can help to distinguish PS-
specific habits (=character) of TEMPERAMENT & CHARACTER > self-report: 35-45min disorders
adjustment & which expresses a > Likert scale: give score based on if
Cloninger = psychiatrist
characteristic mode of individual you (dis)agree with statement
reaction to his surroundings → interested in PS, but more in how ≠ in B is
wired + how we react > 240 T/F
(=temperament) → tool looks more in detail at
→ did a lot of things:
personalities
, perfect balance? principle last 2 test = conflict
SCORING PERSONALITY
→ rodents chose between safe – not
TRAITS IN RODENTS safe environment
→ conflict between exploring &
HOLEBOARD TEST potential threatening environm.
animal put head in dark holes
→ count #head dips + how many ≠ holes
NEUROCHEMICAL ANALYSES
~ how much animal explores new OF NT
PS-TRAITS & NEURO- environment 2 methods:
I. HOMOGENATES: sacrifice animal ->
TRANSMISSION CANOPY TEST take B -> homogenize -> add compound
NOVELTY SEEKING have canopy (onderdak) where animal can to extract NT -> homogenize -> HPLC
= heritable tendency toward intense crawl under & explore or UPLC -> chromatography: see NT
excitement → measure how long till animal comes from or NT-metabolites
→ stimulates to seek something new under canopy + how much time under
that gives reward or to stop some- NT determine aspects of personality canopy & open parts here you take all NT present in tissue,
thing that is perceived as negative → everyone genetic variations in NT-systems also presynaptic ones (are not yet
(relief of punishment) → can explain PS ≠ DARK-LIGHT influencing animal behavior
→ behavioral actions aiming at II. MICRODIALYSIS: measures only NT in
BIOGENIC AMINES TRANSITION synaptic cleft -> only these have
> avoidance monotony (eentonigheid)
> pursuit potential rewards BOX influence on behavior
> active avoidance punishment 2 compartments: → so only NT present when animal
> small & black was showing specific behavior
> open & bright are measured = big advantage!!!
→ measure latency for 1st entry in
bright part + time spend in light-dark > need constant flow perfusion fluid
SYNTHESIS & BREAKDOWN NT of ACSF
HARM AVOIDANCE → use of probes with semi-
= heritable tendency to respond intensely INDOLAMINES
ELEVATED PLUSMAZE permeable membranes: occur
CATECHOLAMINES:
to signals of aversive stimuli Phe → Tyr → DOPA → 2 open bright arms & closed compartment osmosis
→ behavioral inhibition aiming at: DA → NA → A Trp → measure time light-dark compartment > surgical procedure to plant probes
> avoiding punishment > in vivo awake animals
> avoiding novelty DOPAC MHPG 5-HT OPEN FIELD TEST → so direct link between NT
> avoiding nonreward release & animal behavior
measure where animal walks
→ helps to prevent dangerous HVA → does it explore? or stay put?
situations when chose which technique?
→ where is it walking? safe place ~ edges? homogenates: can look at more B-regions
REWARD DEPENDENCE or center room? in same animal
= heritable tendency to respond intensely → microdialysis limited bcs of skull +
to signals of reward, particularly: verbal acclimatization period needed to live
signs of social approval, help/relief & sentiment with probe
,so choice depends on research question conclusion study:
→ deep B structures = homogenates !!! DOPAMINE ANTAGONISTS > white = animals in home cage = controls GLUTAMATE
= inhibition dopaminergic N > black = animals put in open field set up conclusion study:
DOPAMINERGIC eg. clozapine = neuroleptic compound = → exploration I: in both cortex & hippo- glutamate = excitatory NT
PATHWAYS flattens emotional response: campus Ach↑ → modulate cortical & hippocampal
> ignore stimuli → exploration II: slight ↑ & then ↓ cholinergic activity
≠ dopaminergic PW !!! for behavioral > spontaneous activity & speech↓ → but no role in exploration new
activation & NS: → apathic behavior so: environment & habituation
> nigrostriatal
> associative ability & seeking -> Ach follows level of exploration: role
> mesolimbic/ventral mesostriatal ENDOCRINOLOGY: HPA-AXIS
behavior ↓ in motor activity
> mesolimbocortical
> mesodiencephalic -> Ach !!! NT to activate explore new environment = stress
OTHER PATHWAYS activation & not only dopa!!! → HPA-axis control mechanism stress
researchers also interested in other NT response
NIGROSTRIATAL → animal based study: link Ach, GABA & → animal study: NS in correlation with
= substantia nigra --> nucleus caudate & glutamate to behavior HPA-axis (elevated plusmaze)
putamen (=dorsal striatum): → methodology: → saw:
> part of basal ganglia loop > behavior: open field test: > high responders (HR) = rats
> responsible for limb movement a) 30min open field = exploration I exhibited locomotor counts
→ PW degenerated in Parkinson → highest activity level first in highest 3th of sample
→ movement problems 10min & then declines > LR = “” lowest 3th of sample
b) 60min home cage
MESOLIMBIC c) 30min exploration II
= ventral tegmental area --> → first 10 min ≠ with
→ limbic structures (hippocampus, exploration I GABA
amygdala & septum) -> regulation d) 60min home cage
emotional responses conclusion study:
> neurochemistry: microdialysis
→ complete neo-cortex -> motivational > exploration I: slight ↑, but not significant
behavior from controls
CHOLINERGIC PW: Ach > exploration II: negative correlation cortex
PHARMACOLOGICAL = basal foreB nuclei -> limbic system, hippo- GABA & motor activity exploration II
campus, complete neo-cortex & diencephalon → the more GABA, the less animals move
INTERVENTION = B-stem nuclei -> diencephalic B regions, → GABA = behavioral inhibition & role A) latency to enter light compartment
intervene with B mechanisms with agonist lower B regions & spinal cord in habituation → HR entered faster light
& antagonists → main source cholinergic NT ~ Ach B-C) how much time spend in light part
DOPAMINE AGONISTS → HR longer in light
> role cognitive tasks: LTP (learning & D) results elevated plusmaze: time
= stimulation dopaminergic N memory) spend open arms, closed arms & middle
eg. L-dopa: > !!! for response new stimuli: puts new open part
> locomotor activity ↑ info in B -> next time to new stimuli → HR > open arms
> feeling of joy & satisfaction ↑ you’re going to recognize it
→ LR > closed arms
> can reinforce drug effects > sleep
, influence on dopa release in system:
PLASMA CORTICOSTERONE EtOH DEPENDENCE dopa release VTA↑↑
LEVELS human based study: tried to link risk of → gives addicted feeling
killed animals to sample B regions & becoming alcoholic ~ NS
determine HPA related parameters ~ → looked at: COCAINE ADDICTION
corticosterone levels: > medium risk families = brother/sister rodent based study -> did 2 things:
A) comparison HR & LR: addicted, but parents not > wheel running: after running cocaine
> high risk families = both brother/sister
> before experiment: no ≠ administration
& parents addicted → HNS more on the wheel then LNS
> during experiment: HR↑ → subdivided based on EtOH usage:
B) restraint: induced other stress to COMPLETE HPA-AXIS -> moderate drinkers
rule out that response was a general -> problem drinkers
response to stress HR & LR ≠ stress systems?
-> alcohol addicts
→ no ≠ HR & LR → each group tested with
personality questionnaires
conclusion: animals exposed to focused on NS
general stress = no ≠ → high NS score = high risk > self administration: probe in animals
→ animal in plusmaze (control alcohol usage -> push handle -> cocaine directly
own response) = significant ≠ → link personality ~ risk infused in reward system
→ HPA-axis role in NS & becoming addict • first maintenance phase: animals
cause ≠?
aspects of personality knows handle releases cocaine
> (epi)genetic?
> maternal behavior?
NICOTINE ADDICTION → HNS push handle more
> environment? rodent based study: does nicotine act on → addiction risk ↑
B-reward system? • then reinstatement period:
PATHO- HNS & LNS given saline instead of
PHYSIOLOGY first holeboard: cocaine → then followed by 1
> #head dips ~ NS → high NS >> head dips cocaine dose → HNS start pulling
MR & GR mRNA LEVELS OF NS > #holes visited ~ anxiety handle wayyyy more
hippocampal mineralocorticoid R & gluco- !!!! PW = mesolimbocortical: activated bcs of → link personality ~ risk addiction
corticoid R also !!! HPA parameter: then animals exposed to normal H2O & nicotine
positive rewards
A) GR: HR < LR solution
→ neurocircuitry of reward: ventral
→ ↓GR expression responsible for → nicotine consumption: HNS >> LNS
tegmental area -> PFC -> nucl. accumbens
lower anxiety HR rats? → did internal control to see if animals
& amydala
→ gave GR antagonist to LR that consumed more, were bigger &
→ anxiety ↓: >> exploration addictions stimulate dopa release in PW just needed more -> was not the case
→ other indication that → HNS = risk becoming nicotine addict !!! handle not always active (would over-
there’s a link between dose)
stress & personality
EFFECT NICOTINE → work with light: light on? = can
B) MR = regulation basal secretion cortico- nicotine influence dopa reward system via administer cocaine / light off = no
sterone → no ≠ HR & LR cholinergic system cocaine
→ nicotine can replace Ach & activate R → need a learning period
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