Neuro mod 3 Flashcards
process of acquiring new info, behavior patterns or abilities , characterized by modifications of behavior as a result of practice, study, or experience
-systemic relatively permanent change in behavior that occurs through experience
*dependent on ability to take in info from outside & process it
learning
ability to retain info based on mental process of
1. learning of ENCODING
2. RETENTION across some internal of time
3. RETRIEVAL or reactivation of the memory
memory
very brief stores sensory impression of scene
iconic memory
form of memory that usually lasts a dew seconds as long as its rehearsed
-closely tied to working memory –> holding information in mind
short-term memory
a form of memory that outlasts short term memory (STM) but not LTM
intermediate memory
enduring form of memory that lasts days, weeks, years
includes:
-episodic
-declarative
-nondeclarative
long term memory
-knowledge about world – FACTS anyone can know
-info about an area of expertise
-general knowledge
things learned in school
*I KNOW
semantic memory
-info is autobiographical
-the what where when & how
-*I REMEMBER
ex. fav halloween, losing 1st tooth, etc.
episodic memory
info is verbally communicated that helps you remember
declarative/explicit memory
things you know by doing it
non declarative (implicit) memory
learning to perform a task that requires motor coordination
-form of non declarative memory
procedural memory (skills)
phenomenon by which exposure to a stimulus facilitates a subsequent response to the same or similar stimulus
-change in how you process stimulus based on the prior exposure to same stimulus or similar stimulus
priming
form of learning by which an organism comes to associate 2 stimulus & a response
classical conditioning
-severe seizures
-got rid of hippocampus
-partial retrograde amnesia
-complete anterograde amnestia
-can do STM tasks
-can form implicit memories
He could:
-digit span –> succeed if allowed to rehearse (shows he has STM)
-recall early life events
mirror drawing test –> couldn’t remember task but got better
-eye blinking conditioning
H.M.
-novel stimuli
-emotional stimuli
-large objects
-vividly colored objects
-things moving
Encoding
-attentional processes
likely to remember these things
noting physical features of a stimulus
shallow
giving the stimulus a label
intermediate
thinking about the meaning of the stimulus
deep
memory system that holds info temporarily as we perform cognitive tasks
*caudate nucleus –important for retaining a motor response
*visual cortex – important for recognition of objects/visual stimuli
*hippocampus – important for spatial recognition (location)
working memory
important for recognition of objects/visual stimuli
visual cortex
important for spatial recognition (location)
hippocampus
important for retaining a motor response
caudate nucleus
-try to remember if you saw something before
-activation in the left hemisphere frontal cortices
-rehearsal of info via the phonological loop
N-back task
-binding of info occurs in __ ~3 days then ,over to frontal regions
-memories are temporally stored in the ___ but shift to cortical areas for long term memory storage
importance of hippocampus
memory widely distributed but different loci store different aspects of while
connectionism
what lobe is important for episodic storage
anterior frontal lobe
what lobe is important for semantic storage
-posterior frontal lobe
-temporal lobe
-stem completion task
-priming based on visual word form
-reduced activation in the occipitotemportal cortex
perceptual priming
-false memory task
-priming based on word meaning
-reduced activation in left frontal cortex
conceptual priming
involved in planning + problem solving
*rely based on ganglia
skill memory
- involves the encoding of relationships between events, for example, between two stimuli or between a stimulus and a response
-cerebellum
-activation increase in hippocampus
associative learning
hippocampus + cortex b/c needed for declarative memory
complex association
stable + enduring increase in effectiveness of synapses following repeated, strong stimulation
possible mechanism for learning + memory at neuronal level
Can occur:
invertebrates + vertebrates
-many brain regions
long term potentiation
-synaptic connections stronger and more effective
Bliss + Lomo
- NTs (glutamate – important for learning and memory) released from presynaptic neuron
- NTs bind to receptors on postsynaptic neuron
- affect channels (AMPA & NMDA) on postsynaptic membrane
LTP occurring early stages
- glutamate binds to NMDA & AMPA receptors
- AMPA channels open, Na+ comes into cells
-NMDA receptors blocked by Mg2+ –> voltage dependent + needs increased depolarization to remove block otherwise no LTP - Mg2+ removed with sufficient depolarization
- once Mg2+ removed –> Na + Ca –> postsynaptic neuron
- Ca2+ activates CAMKII (protein kinase that alters or activates other proteins)
- CAMII
- adds AMPA Chanels into neuron membrane –> causes nearby AMPA channels to move to synapse –> increases conductance of NA+
*ADDED AMPA CHANNELS –> glutamate can bind to postsynaptic neuron
*increase singling ability
*lasts 1-3 hours - along with CAMKII Ca2+ activates other protein kinases
- these kinases act on CREB (transcription factor – binds to promotor region – change in gene expression)
- CREB tells neuron to make: (kinases, receptors, & dendrites)
specifics of late LTP
- new synaptic connections
- greater signaling ability btw existing neuronal connections
- reshaping of neuron
*renders LTP relatively permanent
late LTP gene transcription effects
-retrograde messengers released from postsynaptic cell
-signal presynaptic cell to release more NT
effects of presynaptic neuron
- threshold dependency: LTP can happen if neuron has repetitive stimulation –> allows is to learn form repetitive info
- Input specificity: only want to make connections between pieces of info that should be connected
- LTP doesn’t affect neighboring synapses that aren’t active - associativity: do want association of certain info (ex. classical conditioning)
-if neighboring pathway is being strongly stimulated, both synaptic pathway undergo LTP
properties of LTP
process by which specific sets of synopsis are selectively weakened
-low level activation for extended time
-smaller EPSP
long term depression
- glutamate binds to NMDA + AMPA receptors
- AMPA channels open Na+ in cell
- Mg2+ remove with sufficient depolarization (-35 mv)
- once mg2+ is removed Na+ + Ca2+ –> postsynaptic neuron
- Ca2+ activates calcineurin
-protein phosphates alter other proteins + removes phosphate groups - calcineurin activates protein phosphates (PP1)
- calcineurin & PP1 act on AMPA receptors in membrane to remove them
*calcunerurin has higher affinity for ca than CAMKII
*amt of CA2+ determines LTD or LTP occurring
specifics of LTD
dendrites shrink or disappear
-process complex: some signaling may rely on proapoptic mechanisms
specific of LTD
brings together biological, psychological, and sociocultural features to understand abnormal behavior
biopsychosocial model
-most common psychosis: severe mental disorder
-broad spectrum of cognitive + emotional dysfunction
-can disrupt perception, thoughts, speech, & movement
-diagnosis based on behavioral symptoms
schizophrenia
system of beliefs that would be seen by most members of the society as misrepresentations of reality
-grandeur + persecutions
*FALSE BELIEFS
delusions
experience of sensory events without any inout from surrounding environment
-auditory ____ is most common
hallucinations
erratic speech
disorganized speech
erratic motor behavior + emotional reactions
-catatonia: waxy effect
gross disorganized or catanoic behavior
-emotional + social withdrawal
-apathy
poverty of thought/speech
negative symptoms of schizophrenia
-delusions
-hallucinations
-disorganized speech
must have 2+ symptoms during 1 month period to be diagnosed with schizophrenia
-large ventricles –> atrophy or damage to brain areas bordering ventricles
-neuronal inputs + outputs are disorganized
Smaller:
-hippocampus
-amygdala
-entorhinal cortices
-hippocampus
-cingulate cortex
-prefrontal cortex
structural differences in SZ
less metabolic activity during difficult cognitive task
-function difference in SZ
hypofrontality hypothesis
What causes differences in psychopathology
-genetic + environmental factors
-likely gene-environment interactions –> epigenetic effects
-genes responsible for making some individuals vulnerable to SZ
-children w/ biological parents w/ SZ –> increase of SZ
-If MZ twin w/ SZ –> -48% chance
-DZ twin w/ SZ –> 17%
SNPS
-regulate expression of genes upstream or downstream of loci
-impact non-protein coding genes
Genetic vulnerability for SZ
-whether particular genes associated with particular traits
-SNPS + SZ
*no confirmed casual mutations underlying SZ
genome wide association studies
-monozygotic
-onset, symptom diagnoses, disorder, outcomes differ
case of genuine quadruplets
dopamine system too active (hyperdopaminergic) in individuals diagnosed w/ SZ
-not an issues w/ clearance at synapse
-not issue of too many D2 receptors
-more tyrosine hyroxylase –> D2
Evidence
-Amphetamine use
-treat with resperine
-treat Parkinson w/ L-Dopa
dopamine hypothesis
leads to increase conc. of DA –> increase psychotic symptoms
amphetamine use
decrease extracellular concentration of DA –> no psychotic symptoms
-deletion of monoamines = depressive symptoms
-deletion of tryptophan (precursor for 5-HT) –> depressive symptoms
resperine
-antagonists at D2 receptor –> lack of effect + NTs can’t act
-to be effective, drug must bond optimal # of D2 receptors
-<50% – little to no response
-75% – risk off extrapyramidal side effects increase
- > 50% – increase response
antipsychotic
DA plays role in assigning motivational salience to internal or external stimuli. In this swat DA determines which stimuli grab our attention + drive behavior
abberent salience model
- elevation of DA –> release in absence of appropriate stimuli
- dysregulated release leads individuals to attribute salience to irrelevant stimuli
- everyday occurrences imbued w/ sense of inexplicable significance
- individuals build delusion based around these occurrences
relation of DA dysregulation + symptoms
- DA dysregulation
- increase “noise” in system & drowning out DA signals linked + reward
- reduction in motivation drive
- social withdrawal + neglect of interest
negative symptoms of SZ
-1/3 patients don’t show or late response to increase D2 receptors occupancy
- too much DA in striation
-not enough DA in prefrontal cortex
-suggest more than just DA system involved
problems w/ DA hypothesis
-interaction btw DA & Glu systems
-NMDA antagonists can influence DA synthesis + firing patterns
glutamate disorder
psychological primary disturbance of mood
-fundamental experiences of depression + mania contribute to mood disorders
mood disorder
-most commonly diagnosed depressed
-most severe depression
*symptoms must persist for at least 2 week
-characterized by physical changed + emotional shutdown = +/- sleep
*too little monoamines
treatments: MADIS, TCA, SSRIs, + CBI
symptoms:
*reduced interest or pleasure in all or most activities: anhedonia
-physical changes
-behavioral/emotional shutdown
Major Depressive Disorder
-size reduction in limbic + cortical structures:
-hippocampus
-obitofrontal cortex
-sub-genual prefrontal cortex
-episodes longer + multiple related relapses
amygdala sizes vary
-enlarges onset and reduced as progressed
-move pronounced reduction in women
structural differences in MDD
-hyper activation of HA axis: feedback loop for responding to stress
-potential role in volumetric changes in hippocampus, OFC, PFC, & amygdala
-mood congruent emotion processing bias: hypersensitive to negative stimuli & hypostimuli to positive stimuli
-lack of ability to regulate negative emotion
– less activation in dorsolateral prefrontal cortex
–involved in emotion regulation + executive control
Functional differences in MDD
-2-3x more likely to have depression if fam member has been diagnosed
Mz: 60% DZ: 20.2%
adoption: increase likelihood of developing depression of biological parent diagnosed
genetic factors of MDD
most strongly associated with occurrences of MDD – involve ed in the circadian rhythm
RRA gene
-low SES (socioeconomic status)
-minority women
-situational factors
-minority women
-dysregulation of NT: monoamine hypothesis (NDR, DA, H-5A
environmental factors for MDD
food with increase tryptophan – can’t break down in gut –> hypertensive crisis + dietary restrictions
effects of MAOI
increase monoamines = no depressive symptoms
TCA effects
MAOI break down monoamines
-antipsychotic
-MAOIs block the action of MAOs degradation of monoamines
iproniazid (MAOI)
tricyclic antidepressant (TCA)
-block reuptake of 5-HT + NE –> evidence of monoamine dysregulation
-antipsychotic
-increase monoamines = no depressive symptoms
imipramine (TCA)
-main drug to treat depression
-more selective in how they act MAOIs or TCAs
-fast acting
-help in stages
1. normal action of autoreceptors –> decrease 5-ht release at synapse
2. when SSRIs act autoreceptors over activated –> also down signal –> slow down 5-HT release
3. autoreceptors become desensitized after few weeks –> increase signaling
effects:
-50% decrease in firing rate
-ventral tegmental area normally fires in response to neurons –> decreased in patients on SSRIs
-decrease in response to chocolate
-decrease in reward processing
development of SSRI (selective serotonin reuptake inhibitors)
1/3 of patients don’t respond to treatment
problems with monoamine hypothesis
-reshape interpretation of life (what kind of therapy?)
-often used in combo with antidepressant –> increase improvement
-kind of thoughts + beliefs you have about situations contributing to hopelessness
cognitive behavioral therapy
involves fears that are uncontrollable, disproportionate to actual danger that person might be in & disruptive to ordinary life
anxiety disorder
negative mood state characterized by bodily symptoms of physical tension by apprehension about FUTURE
anxiety
-2-5% of pop meets criteria for GAP during 1 year period
-6% at some point during lifetime
-most common anxiety disorder
-2/3 women – changes by culture
*marked by persistent anxiety for at least 6 months
*individuals unable not specify source of anxiety
*TREATMENTS –> BZI
GAD
-interest in amygdala – fear circuit region
-increase gray matter
-prefrontal cortex larger
-reduction in hippocampus
-increase functional manners for FAD than structural `
structural differences in GAD
-decrease connectivity btw amygdala + PFC
-decrease connectivity btw amygdala & anterior angulate cortex (ACC)
-increase activation of PFC when presented with worry statements
-increase activation of FFC when presented with worry statements
functional differences in GAD
-genetic + environment
-NT dysfunction
what causes these structural and functional differences in GAD patients
15% of people with relatives diagnosed with GAD also have GAD
twins
MZ: 21.5%
DZ: 12.5%
-genome wide association studies
genetic factors of GAD
perceive world as dangerous/out of control
-life stressors
environmental factors of GAD
lacks ability to inhibit worry/anxious feelings
NT dysregualtion hypothesis
-act on GABA signaling system
-GABA is mainly inhibiting NT in CNS
*increase concentration of GABA receptors in cortex & limbic system
-decrease excitability of neurons + produces calming effect on brain
-positive (agonist) allosteric (indirect) modulator at receptor site
-GABA receptor complex has 5 subunits
-2 GABA binding sites
-1 BZD binding site
-BZD binding –> changing receptor confirmation –> increase in GABA affinity
BZD action
-modulates binding of GABA
-increase cloning coming into neuron –> IPSP
benzodiazepines (BZD)
-stop taking –> anxiety returns
-take in large doses = physical dependence
bad side effects:
-depression
-memory loss
-aggressive behavior
-lack of coordination
-interacts with other substances ex. alcohol
*good for short term
*only take for ~1-2 weeks
problems with BZD
-anxiolytic –> developed as antipsychotic
-approved for GAD
-5HT partial agonist
-g couple protein –> inhibiting effects
Buspirone
system of advantaged based on race that is created and maintained by an interplay btw psychological factors + sociopolitical factors
*race meaningful by 9 yo
racism
-a collectokin of individuals who have at least 1 attribute in common but otherwise doesn’t necessarily interact
-used to conceptualize in groups + out groups
-preferring “like me” starts early
social category
mere exposure to people form a group increase liking for characteristic of that group
familiarity (contact) hypothesis
taught explicitly or implicitly to attend race as meaningful category
minimal group hypothesis
groups can be formed cause of?
-group labels
-visual markers of groups (ex. t-shirts)
*type of language used – using as an individual or group?
leads children to infer proteins applies to ALL category members
-sterotypes can be passed across genetic by parents ‘likelihood’ of generic language
generic language
any state of mind, feeling , or behavior that criticizes others on account of social group to which they may belong to
prejudice
widely held belief about a group
stereotyping
unjust or prejudicial treatment of different cauterizes of people
discrimination
-measures strength of association between concepts, evaluations, or sterotypes
-participants sort words or images into categories
-if have implicit bias tp associate white with w=good and black with bad, it’ll take longer to respond to stereotype incongruent trials
*strength of bias reflected in difference in RT btw those types
implicit bias test (IAT)
Hierarchal control model:
Stage 1: low level (mostly) automatic processing
-detects categorizes, evaluates race
Stage 2: higher order processing
-exert control over bias reactions
-achieve personal + societal goal of combating racism
Processing someone’s race
-fusiform gyrus located in ventral occioototemporal cortex –> Fusiform face area (FFA)
-sensitive to faces
-increase activation to in-group than outgrip faces in FFA
*enhanced processing in group members
face encoding
posterior cingulate PCC
-activated when retrieve info about PEOPLE WE KNOW
-increase activation to strangers in in-group than outgroup
posterior knowledge
-representation of social knowledge
-acitvation when categorizing based on stereotype relevant judgement
-lots of connections to VMPFC
anterior temporal lobe
-social information processing
-sensitive to humanness
-theory of mind takes
-lack of VMPFC activation = dehumanization
vental medial PFC
amygdala: almond shaped structure in medial temporal lobe, part of limbic system
-emotional learning + memory
do you feel a threat?
increase activation when:
-direct eye gaze
-judgement made in context of threat
-presentation is brief
*amygdala activation reflects more than processing of perceptual features
ERPs: show preaches of race in 1/10 of sec
increase amplitude for out group members
-greater response = vigilant attention to potential threat
-increase effect in those with stronger implicit prejudice
amygdala
make decisions based on center item, ignoring other items
*longer response times on incongruent trials
flanker task
-*MONITORS FOR RACIAL BIASES
-monitors for conflicts in automatic + intentional responses
-when conflicts occur, executrices control is engaged
*monitor what is going on
-event related negativity (ERNS) is an ERP response widely associated with ACC engagement
-individual internally motivated to non-prejudice show increase ERNS when stereotype incongruent error on stoop like tasks
anterior cingulate cortex
-regulating racial biases
-top down control of sensory + motor representation activation in working memory
-cognitive regulation of emotions can modulate amygdala response
-may be engages to inhibit implicit race attitudes during interactions with racial outgroup members
dorsal lateral prefrontal cortex (DLPFC)
