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Psych 202 exam 4

chap. 15, 17 and 18 543-559

Emotional response Emotions are physiological responses to a salient(events that stand out the most) environmental situation objective 3 types(all automatic): Autonomic arousal, Behavioral/action, motivation can be measured Subjective 1: feelings can be measured
Autonomic arousal emotional response Objective automatic response Nervous system response to the situation, stress -Mobilizes energy for quick response and Hormone release reinforces the autonomic response
behavioral/action emotional response objective automatic responses to a situation -Physical movements in response to a situation, different between species -defending or attacking in response to a threat
Motivation emotional response objective automatic response -Psychological driven to overcome an adaptive challenge -Directs the behavior driven to avoid pain & move towards pleasure, gives the directions to correctly use behaviors
Feelings emotional response Subjective component of emotions, humans feel as they experience -The feelings described as "emotions" have been associated w/physiological responses through learning/experience -can't be measured, only talk to humans about feelings
James-Lange theory Feelings arise from sensory feedback about the physiological response, brain interprets feedback= feelings, emotions caused by the bodily changes -Ppl w/ spinal cord problems get varying degrees of feedback, more damage= weak emotions/muted feelings
Cannon-Bard theory Emotions help us deal wit the environment Feelings are triggered by the cortex, parallel w/ physiological responses, criticized james -Claiming that the experience of emotions starts before the autonomic changes, which are relatively slow -Bodily response/emotional experience are simultaneous
Schacter theory Feelings result from the cognitive interpretation of physiological activation, like james -Interpret by eliciting stimuli, the surrounding situation, cognitive states (body/situation) -emotional labels depend on the interpretations of a situation
Fear Very easy to model, emotional response to a perceived threat -Amygdala is central to fear, reactions to stimuli w/biological significance(smelling smoke)
Amygdala and fear response Involved in reactions to stimuli w/biological significance(like needing food/water) -Receives input from: thalamus(pulls in all sensory signals, doesn't interpret,get info before brain), Sensory cortex(interprets stimuli), hippo(memories about stimuli)
Central Nucleus of the amygdala responses to fear integrates incoming sensory info, projects fear to Gray(behavior), Lateral(autonomic/feeding), BNST(hormonal) -Critical to emotion provoked by aversive stimuli=increase in activity -Artificial stimulation produces signs of fear/agitation (no stimuli)
Thalamus in fear Sends input to the amygdala about sensory signals but doesn't interpret, receives info before the brain interprets
Sensory cortex in fear Sends input to amygdala about the interpreted stimuli
Hippocampus in fear Sends input to amygdala about memories about stimuli
Periaqueductal gray area in fear Receives info from Central nucleus of the amygdala Behavioral response
Lateral Hypothalamus in fear Receives info from CN of the amygdala Autonomic (sympathetic) response, feeding behaviors
Bed nucleus of the Stria terminalis (BNST) in fear Hormonal response
Lesions on CN of amygdala (rats) result in loss of fear to aversive stimuli -no fear, really melow animals -Tame animals, fewer stress hormones, decreased anxiety, less stress,induced illness -fear is the reason animals react badly
Lesions on CN of amygdala (humans) Unable to recall emotional memories Unable to learn conditioned emotional responses
Kluver-Bucy syndrome removal of amygdala = loss of fear removing large portions of the temporal lobe animals become tame plus eat random things plus hypersexuality
Conditioned emotional response (other selections of the brain, but takes very long) Central Nucleus of Amygdala role in aversive emotional learning -Neutral sti. + Fear-inducing sti. = learned fear response to the neutral sti. ex. tone plus shock= tone causes fear -CNA is destroyed, animals won't learn this conditioned emotional resp.
Aggression Behavioral response involving threatening gestures or an attack on another animal -Species-specific, controlled by genetically organized neural circuits related to both reproduction/self defense -Circuits are very hormone sen. -Controlled by PAG
Periaqueductal grey in aggression Neural circuits located in this area control aggression -receives info from amygdala, medial(male sex behaviors), lateral hypothalamus (eating)
Dorsal PAG in aggression Controls defense behaviors
Ventral PAG in aggression Controls eating, hunting behaviors
Prefrontal cortex Regulates emotional expression (keep things in check) -recongnizes the emotional significance of complex social situations -Inhibits impulses,reg. behavioral responses Slowest developing area of the brain,
Impairment of prefrontal cortex (humans) results in faulty emotional regulation (didn't develop correctly/damage) -Poor impulse control, aggression/violence
Antisocial Personality disorder (humans) Correlated w/a reduction in gray matter of the prefrontal cortex
Oritofrontal cortex Part of the oritofrontal cortex Critical to emotional regulation Damage: lack of emotional regulation, impaired planning, social res., impulsive aggression/violence
Medial prefrontal cortex Part of prefrontal cortex Critical to emotional reasoning, contributes to emotional/moral res. -How we chosen to express our emotions/they play into our morals
Serotionin in aggression Inhibits aggression/risk taking behavior -Low 5-HT activity increase aggressive attacks
Monkeys + serotonin Juvenile monkey's w/low 5-HT show increased risk-taking behavior/aggressive attacks on dominant monkeys -Impulsive behavior= death
Mice + Serotonin Mice lacking the 5-HT receptor exhibit increased aggression on other mice
Prefrontal serotonin in aggression Inhibits aggression/impulsive behaviors Low levels: correlated w/aggression, assault, arson, murder, child abuse -Agonists decrease irritability, aggressiveness/impulsivity on psychological measures
Hormonal control of aggression Prenatal androgen exposure organizes neural circuits controlling aggression -puberty, testosterone activates these circuits, increasing aggressive behaviors
Medial preoptic area Critical to reproductive/defensive behaviors -sti. Testosterone produces aggression (High con. of androgen receptors, injections= increase intermale aggression)
Castration not aggressive can't get aroused
Androgen antagonists chemical castration cuts of source of androgen so won't work on receptors, decreased aggression
High levels of androgen like prison pop. high levels of aggression
Anabolic steroids increasing aggression
Androgens correlations don't indicate that increased androgen causes behavior no causal studies in humans
Communication of emotions Emotion is communicated through physical responses -Alerts others to one's feelings, includes postural changes, sounds and facial expressions *most intense w/audience
Facial expressions Innate responses, automatic/involuntary -RIght hemisphere is critical to expression of emotion -Darwin: ppl of isolated tribes recognize the meaning of facial expressions /make the same expressions -Blind children
Innate responses Unlearned physical responses to specific emotions -Biologically inherited, not learned
Right Hemisphere of brain Critical to expression/recognition of emotion -left side of the face makes more intense expression then right -lesions impair facial expression/recognition of emotion
Mirco expressions a lot of expressions that escape prefrontal can't stop it
Facial muscles 1:facial nerve innervates superficial muscles(attached to facial skin) of expression 2:trigeminal nerve innervates deep facial muscles(attached structures of the head) jaw
Paralinguistic major role of facial expression -Face accessory to verbal communication= emphasis/direction of combo
Recognition of emotion Visual/auditory, innate -Facial expression, tone of voice/words -right hemisphere is critical to recognizing/understanding emotion, damage impairs both -AMG: fear, activity increases when viewing pic of faces expressing fear, damage: impairs ability
Stress Physiological/psychological response to a situation(not emotion) -General adaptation syndrome -Hormones: corticosteroid ex. cortisol from adrenal cortex
General adaptation syndrome Connection between stress/disease -Alarm response: initial res. to stress -Adaptation stage: 2nd activation of appropriate response systems/reest. of homeostatic balance -Exhaustion stage: increased susceptibility to disease
Cortisol released in response to a threat(stress) by adrenal cortex -Inhibits immune function -Long-term consequences
Immune system Brain sti. immune function -Organs-thymus,spleen,lymph nodes,bone marrow produce: Phagocytes,B/T lymphocytes, Helper T cells -Monitored/regulated by brain cytokine receptors on the vagus nerve
Phagocytes eating cells like macrophages/neutrophils are specialized in engulfing/destroying germs -told what to attack by lymphocytes
B Lymphocytes White blood cells made in the bone marrow :produce proteins= antibodies
T lymphocytes formed in thymus gland act as killer cells -Specialized cells: T helpers secrete cytokines = proteins that regulate activity B cells divide or die
Learning Set of processes by which experience creates enduring changes to neural circuits, changing behavior = memories
Synaptic plasticity Changes in synaptic structure/biochemistry -Changing the strength with which affects the post target
Long-term potentiation(strengthened/increased effect) Strengthening of synaptic connections results from repeated synaptic activity paired w/AP in the postsynaptic neuron -we need to repeat things before we are going to remember it
LTP characteristics Synaptic transmission is more likely to cause an AP in the post-synaptic neuron -last from several mins to years can be induced throughout the brain
LTP modeled/hippocampal formation part of the limbic system located in the temporal lobes -Composed of Dentate gyrus, CA 1-3, subiculum Perforant pathway:
Perforant pathway cell body in the entorthinal cortex synapses w/ the dentate gyrus (door way into/out of the hippo) -major source of input
Experimental induction of LTP Sti. electrode in the perforant pathway, recording electrode in the dentate gyrus =1 burst of sti. delivered to the perforant pathway = AP -Resulting EPSP recorded in the dentate gyrus= baseline for normal synaptic firing strength
Experimental induction of LTP part 2 Induce LTP=rapid burst of electrical pulses is delivered to the perforant pathway (~100 pulses/2sec) then wait -Detect: single, short sti. burst delivered to the perforant pathway Pop. (cells surrounding the electrode) EPSP measured in dentate gyrus
Pos. LTP induction An increased response in the dentate gyrus indicates that synapses have been strengthened -One AP is more likely to get the cells to depolarize
Neural events resulting in LTP Synaptic strengthening depends on: NT binding at the synapse + depolarization of the post-synaptic cell(at the same time) -Depolarization of a neuron doesn't strengthen all synapses, only those that are active at the time of depolarization
3 times of Synaptic modifications = LTP Add of receptors/synapses, increased glutamate release from the presynaptic membrane
Calcium Critical to est. LTP -Second messenger= activates protein kinases(direct chemical reactions in the chemical reactions in the cell necessary for LTP) -NT binding+depolarization helps Ca get into cell
NMDA receptors( critical for learning) LTP relies on calcium influx at NMDA glutamate receptors -Ca channels controlled by NMDA receptor are blocked by a Mg ion
Magnesium ejection Glutamate binding + Depolarization of the post synaptic cell -Lets Ca in
Dendritic Spike An AP results in a backwash of depolarization up the cell body/dendrites -Spike+glutamate binding at NMDA receptor= Ca Channels open to allow chemical influx
Increased receptors (Strengthening of synapses) Individual synapses are strengthened by an increase in AMPA receptors on the post.S membrane (increased response to glutamate ) 3 fold increase
CaMK enzymes CA activates CaMK enzymes>activated CaMK binds to an intracellular portion of the NMDA receptor>Linking proteins bind to the CaMK>AMPA bind to linking proteins/are embedded into the cell membrane
Synaptogenesis(LTP result) LTP results in the multiplication of synapses -Most synapses are located on dendritic spines -LTP results in division/multiplication of these spines
Synaptogenesis mechanism (spines expand surface area) Post.S density expands until it perforates=splits into multiple densities>Pre.S active zone splits into corresponding regions>Perforated synapse further divides until the spine branches= 2 spines con. synaptic region
Synaptogenesis results Terminal button of one presynaptic neuron synapsing w/ multiple spines on the Post.S neuron -Increases communication potential between 2 cells 3 fold -2 diff. active zones plus 2 spikes=more synapses
Presynaptic changes LTP ass. w/ an ^ in glutamate release by the Pre.S neuron -Influenced by retrograde messengers: Nitric oxide
Nitric Oxide Retrograde signal from NMDA receptors to the Pre.S membrane -Synthesized in the Post.S membrane in response to Ca influx -Direct messenger tiggers release of glutamate, breaks down quickly very unstable
Hebbian rule wire-strength of synapses between 2 neurons Neurons that fire together, wire together -Synapses that are reliably active just before the generation of an AP are strengthened -Firing weak & strong synapse on the same Post.S neuron> strengthens the weak synapse by association
Classifications of Memory Declarative memory: talk about Nondeclarative memory: hard to talk about, act out)
Declarative memory explicit/readily available to conscious recollection(talk about) -Episodic: memories of events(details) -Semantic: memories of facts
Nondeclarative memory Implicit, unconscious knowledge (hard to talk about, act out) -Perceptual: memory of perviously expeienced stimuli -Motor: Procedural learned behavioral seq. -Stimulus-response:learned res. to specific stimuli
Perceptual Learning association cortex Neural changes that result in recognizing a sti. that has been perceived before ex. recognizing new term -Based on synaptic changes in the sensory ass cortices -Later input from the same stimulus results in the same pattern of activation> recognition sti
Classical conditioning Learning a specific behavioral response in the presence of a give sti. -Response to an ass. between two stimuli -Simple, automatic responses
Classical conditioning: Neural mechanisms Conditioned emotional response: common model of classical conditioning(tone + footshock= freezing behavior -Emotional conditioning relies on Amygdala: LTP exhibited in amygdala following fear conditioning
Areas involved in Classical conditioning Lateral amygdala receives weak input on the CS(tone) & strong input US (footshock) -Strong US synapses depolarize neurons in the lateral amygdala= AP in projections to the central amygdala CNA generates emotional res. (UR freezing)
Hebb's rule classical conditioning Can't use things that we have learned are already safe Repeated depolarization by strong US synapses, paired w/ recep. activation at weak CS synapses=strengthens -Connections between NE signaling the tone/neurons signaling the behavioral res. is strengthened (firing at tone synapse indepent. AP = freeze beha
Motor Learning Procedural memories: changes that result in a new seq. of movements -Est. new motor skill seq., based on changes in motor system -New behaviors req extensive modifi. of brain circuits, adj produce changes to these circuits
Neural control of Motor learning Learning new seq of motor res involves sensory input & motor output -Two pathways: direct transcortical projections Connections through thalamus/basal ganglia
Intital Motor learning Req focus on environmental sti./cortical processing of sensory input accomplished by transcortical pathways
repeated Motor learning Behavior becomes more automatic processing transferred to basal ganglia -Receives input sensory association areas/prefrontal cortex planning -Projects to the prefrontal motor ass. area strengthens connection sensory/motor
Area of motor learning thalamus takes in all sensory before cortex + prefrontal (Planning)> Basal Ganglia -Muscle memory in Basal ganglia(damage motor plans wipe out)
Operant Conditioning learning to make a response in order to gain reinforcement/avoid punishment formation of ass. between discriminative sti, behavioral output, resulting conseq DS= contextual cue
Operant conditioning con. Behavior occurs in res to the DS reinforcing/punishing sti. follows behavior Animal learns to make the correct behavior in that context to gain reward/avoid pain Neural reinforcement mechanism, synapses between DS neurons that produce a behavioral res
Circuitry of Reinforcement Detection of stimuli involves input from regions that project to the VTA Lateral hypothalamus: detects biologically relevant sti, signals presence of reinforcing sti Amygdala evaluates biologically relevant sti. determines the reinforcing value sti.
Circuitry Of reinforcement con. Prefrontal cortex: evaluates stimuli, makes strategies, evaluates outcomes signals that behavior in succeeding VTA makes dopamine
Medial forebrain bundle Axon bundle extends from midbrain to target of the mesolimbic system (amygdala hippocampus nucleus accumbens) passing through the lateral hypo -Primary system involved in reward motivation addiction
Medial forebrain bundle stimulation Highly rewarding Dopamine release in the NAc is strongly reinforcing, just about instant rewards=dopamine=addiction -common model of reward motivation( rat keeps pressing bar just to get instant reward from brain even w/o food)
Neural circuitry of reinforcement Strengthening of synapses by reinforcement Dopamine axons from VTA & glutamate axons from hippocampus, amygdala, prefrontal cortex synapse on the same NAc cells NAc projects to basal ganglia influencing behavioral output Depolarization of NAc neurons by DA strengthens the glutamatergic synapses
Created by: Lizziebell99
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