PSY 209 Exam 4 Study Guide Fall 2024 PDF

**PSY 209 Exam 4 Study Guide** Ch 15 - Importance of having emotions - Helps to experience and evaluate your environment - Helps in interacting and communicating with others in appropriate ways - Emotions are associated with - Overt behaviors (crying, laughter)...

**PSY 209 Exam 4 Study Guide** Ch 15 - Importance of having emotions - Helps to experience and evaluate your environment - Helps in interacting and communicating with others in appropriate ways - Emotions are associated with - Overt behaviors (crying, laughter) - Motivational states (approach, avoidance) - Physiological arousal (increased heartbeat, perspiration) - Theories of emotion and bodily responses - Folk psychology - Emotions cause autonomic responses - James-Lange Theory - Bodily changes cause emotions - Different physiological responses allow for different emotions - Cannon-Bard Theory - Emotions are independent of physiological responses - Schachter's Cognitive Attribution Model - Emotional experiences depend on the physiological responses combined with the context - Experiment with epinephrine injected - Your emotional interpretation of physiological arousal depend on the emotions of others - Lie detector versus brain imaging - Lie detector measures sympathetic responses which may not be specific to lying - Brain imaging can measure specific activation of brain regions linked to lying - Six fundamental emotions - Anger, fear, happiness, sadness, surprise, disgust - Present across cultures - Isolated nonliterate groups show lower levels of agreement on facial expressions showing surprise and disgust - Facial feedback hypothesis - Supports James-Lange theory - Sensory feedback from our facial expression can affect our mood - E.g., putting a smile on your face can make you feel better - Impairment of facial expressions - e.g., Bell's Palsy, Botox - may impair emotional experiences - may have negative effects on social interactions - MacLean\'s limbic system - Group of brain regions involved in emotions - Ongoing debate what brain regions belong to limbic system - Anxiety disorders - When fear responses occur in safe environments - Symptoms are a result of the fear system (mostly amygdala) breaking loose of cortical controls (mostly prefrontal cortex) - Fear conditioning - Involves fear learning in which a neutral stimulus (e.g., tone) is repeatedly paired with an unpleasant experience (e.g., shock) - Subjects now act fearful in response to the neutral stimulus alone - Example of fear conditioning in rats - Neurocircuitry of fear - Fear-inducing stimulus reaches the thalamus - Thalamus projects to the lateral amygdala (Fast road or "Low road") - Lateral amygdala projects to Central Amygdala - Central amygdala mediates fast behavioral/physiological response - Emotion \> Forebrain - Autonomic \> Brain stem - Hormonal \> Hypothalamus - Thalamus projects to the cortex/hippocampus (Slower road or "High Road") - Allows for cognitive appraisal to modify behavioral response - Role of amygdala in fear - Experiments with Patient S.M. showing bilateral amygdala lesions - Fails to recognize fear from facial expressions - Due to failure to fixate on the eyes when viewing facial expressions - Amygdala important for directing attention to relevant emotional cues - Do distinct brain circuits mediate emotions? - Different emotions activate different brain regions - Same brain regions may be active in different emotions - Each emotion is the sum of the relative activation pattern across a network of brain regions involved in emotion CH 16 Part I - Schizophrenia - Positive symptoms (abnormal behaviors that are gained) - Psychosis (key symptom) - Hallucinations - Delusions - Disorganized thought and speech - Negative symptoms (result of lost functions) - Emotional and social withdrawal - Blunted affect or emotional expression - Slow thought and speech - Eye tracking as potential early diagnostic marker for schizophrenia - Eyes of people with schizophrenia move in jerks and fits rather than smoothly tracking a moving object as other people's eyes do - Risk factors to develop schizophrenia - Genetic (e.g., DISC1 gene) - Environmental (stress, immigration, living in cities) - Developmental (e.g., low birth weight) - Epigenetic (Paternal age) - Structural changes in the brain of schizophrenia patients - Lateral ventricles are enlarged - Hippocampus is smaller and pyramidal neurons have disorganized arrangement - Amygdala is smaller - Frontal lobes show loss of gray matter - Hypofrontality hypothesis of schizophrenia - Symptoms of schizophrenia may be caused by underactivation of frontal lobes - Treatments for schizophrenia - Antipsychotics - Block dopamine D2 receptors - Primarily manage/control psychosis - Cognitive behavioral therapy - Manage psychosis - Dopamine hypothesis of schizophrenia - Schizophrenia results from excess in dopamine function - Phencyclidine and ketamine - Simulate almost all symptoms of schizophrenia at low doses - Block glutamate NMDA receptor - Oxytocin (OXT) and social dysfunction in schizophrenia - Schizophrenia patients do not show an increase in OXT after trust-related interactions while control subjects do - There is a positive correlation between accuracy of rating facial emotions and OXT levels in schizophrenia patients - OXT intranasal treatment improved one aspect of theory of mind in schizophrenia patients - OXT intranasal treatment reduced positive but not negative symptoms of schizophrenia CH 16 Part II - Depression - Key symptom is anhedonia - Other symptoms may include sadness, low energy, difficulty concentrating, restless agitation - Treatments for depression - Cognitive behavioral therapy (focus on action-based coping strategies) - Drugs - SSRIs - MAO inhibitors - Deep brain stimulation - Monoamine Hypothesis of Depression - Based on drug iproniazid, that blocks the degradation of monoamines, being effective in treating depression - Deficiency in monoamine function in depression - Problem with hypothesis - Antidepressants work within minutes, but therapeutic efficacy takes several weeks - Stress hormone dysregulation hypothesis of depression - High levels of glucocorticoids may cause depression - Depressed patients show higher cortisol levels on average compared to controls - Dexamethasone suppression test - Used in clinic to evaluate HPA axis in depression - Dexamethasone blocks the release of cortisol in control subjects but is less effective in depressed patients - Dexamethasone binds to glucocorticoid receptors in pituitary - Inhibits the release of ACTH, which in turn results in less release of cortisol - Treatment of Anxiety Disorders - Cognitive behavioral therapy - SSRIs \> increase serotonin availability - Benzodiazepines \> enhance GABA's inhibitory actions - Propranolol \> inhibits actions of norepinehrine - Posttraumatic stress disorder (PTSD) - Impaired fear extinction - Persistent fear memories may be a failure to show fear extinction in safe environment - Hypoactive prefrontal cortex + hyperactive amygdala - Prefrontal cortex may lose effectiveness in suppressing amygdala activity and thus fear responses CH 17 - Impairments in memory - Retrograde amnesia \> loss of memories before onset of amnesia - Anterograde amnesia \> inability to form new memories after onset of amnesia - Patient H.M. - Surgical removal of hippocampus among other brain regions - Could learn motor skills with practice but did not remember performing them - Two kinds of memory - Declarative memory (explicit memory; "what"; e.g., facts) - Semantic memory -- generalized memories - Episodic memory -- autobiographical memories - Non-declarative (implicit memory; "how"; e.g., skills) - Skill learning - Associate learning - Operant conditioning: Response - Outcome - Classical conditioning: Stimulus - Outcome - Memory formation stages - Encoding: sensory information -- short term memory (STM) - Consolidation: transition from STM to long term memories (LTM) - Retrieval: LTM is retrieved, memory becomes plastic - Primacy effect - Better recall for items at the beginning of a list (based on LTM) - Recency effect - Better recall for items at the end of a list (based on STM) - Long term memory storage - Medial temporal lobe (including hippocampus, amygdala) - Crucial for conversion of STM to LTM - LTM are not stored here - Permanent storage tends to occur in brain regions where info was first processed - Memory storage requires physical changes in the brain - Changes in the amount of neurotransmitters released - Changes in neurotransmitter-receptor interactions - Changes in the rate of termination of neurotransmitter signaling - New synapse formation, elimination, or reorganization - Hebb\'s notion of cell assemblies - Ensembles of neurons that are repeatedly activated together could store memory traces - Long-term Potentiation (LTP) - A stable and enduring increase in the effectiveness of synapses - Dependent on activation of NMDA glutamate receptors causing: - Influx of Ca2+ - Activation of CAMKII - More AMPA glutamate receptors inserted into active synapse - Synapse becomes more sensitive to glutamate - Important for the early stages of LTP - Activation of CREB - CREB changes gene transcription rates - Important for longer-lasting LTP and formation of LTM - Artificial activation of an engram in mice - Mice were exposed to fear conditioning in context B - Mice were then exposed to context A - Artificial reactivation of neurons that were active during fear conditioning in context B - Mice show fear response in context A - Turning reactivation off - Mice resume activity = They are not afraid of context A