Neuro mod 3 Flashcards by sophia rahman

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

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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

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very brief stores sensory impression of scene

iconic memory

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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

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a form of memory that outlasts short term memory (STM) but not LTM

intermediate memory

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enduring form of memory that lasts days, weeks, years

includes:
-episodic
-declarative
-nondeclarative

long term memory

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-knowledge about world – FACTS anyone can know
-info about an area of expertise
-general knowledge
things learned in school
*I KNOW

semantic memory

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-info is autobiographical
-the what where when & how
-*I REMEMBER
ex. fav halloween, losing 1st tooth, etc.

episodic memory

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info is verbally communicated that helps you remember

declarative/explicit memory

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things you know by doing it

non declarative (implicit) memory

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learning to perform a task that requires motor coordination
-form of non declarative memory

procedural memory (skills)

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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

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form of learning by which an organism comes to associate 2 stimulus & a response

classical conditioning

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-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.

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-novel stimuli
-emotional stimuli
-large objects
-vividly colored objects
-things moving

Encoding
-attentional processes
likely to remember these things

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noting physical features of a stimulus

shallow

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giving the stimulus a label

intermediate

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thinking about the meaning of the stimulus

deep

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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

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important for recognition of objects/visual stimuli

visual cortex

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important for spatial recognition (location)

hippocampus

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important for retaining a motor response

caudate nucleus

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-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

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-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

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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

1. NTs (glutamate -- important for learning and memory) released from presynaptic neuron 2. NTs bind to receptors on postsynaptic neuron 3. affect channels (AMPA & NMDA) on postsynaptic membrane

LTP occurring early stages

1. glutamate binds to NMDA & AMPA receptors 2. AMPA channels open, Na+ comes into cells -NMDA receptors blocked by Mg2+ --> voltage dependent + needs increased depolarization to remove block otherwise no LTP 3. Mg2+ removed with sufficient depolarization 4. once Mg2+ removed --> Na + Ca --> postsynaptic neuron 5. Ca2+ activates CAMKII (protein kinase that alters or activates other proteins) 6. 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 7. along with CAMKII Ca2+ activates other protein kinases 8. these kinases act on CREB (transcription factor -- binds to promotor region -- change in gene expression) 9. CREB tells neuron to make: (kinases, receptors, & dendrites)

specifics of late LTP

1. new synaptic connections 2. greater signaling ability btw existing neuronal connections 3. 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

1. threshold dependency: LTP can happen if neuron has repetitive stimulation --> allows is to learn form repetitive info 2. 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 3. 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

1. glutamate binds to NMDA + AMPA receptors 2. AMPA channels open Na+ in cell 3. Mg2+ remove with sufficient depolarization (-35 mv) 4. once mg2+ is removed Na+ + Ca2+ --> postsynaptic neuron 5. Ca2+ activates calcineurin -protein phosphates alter other proteins + removes phosphate groups 6. calcineurin activates protein phosphates (PP1) 7. 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

1. elevation of DA --> release in absence of appropriate stimuli 2. dysregulated release leads individuals to attribute salience to irrelevant stimuli 3. everyday occurrences imbued w/ sense of inexplicable significance 4. individuals build delusion based around these occurrences

relation of DA dysregulation + symptoms

1. DA dysregulation 2. increase "noise" in system & drowning out DA signals linked + reward 3. reduction in motivation drive 4. 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)