Emotions, Aggression, and Stress BN8e Exam 4 Review PDF

15 Emotions, Aggression, and Stress Broad Theories of Emotion Emphasize Bodily Responses Folk psychology: emotions cause autonomic responses (like stomach churning) James-Lange theory (1884): - bodily changes cause the emotions we feel - emotions differ due to different physiological r...

15 Emotions, Aggression, and Stress Broad Theories of Emotion Emphasize Bodily Responses Folk psychology: emotions cause autonomic responses (like stomach churning) James-Lange theory (1884): - bodily changes cause the emotions we feel - emotions differ due to different physiological responses Cannon-Bard theory (1927): emotions are independent of physiological responses and help deal with a changing environment Broad Theories of Emotion Emphasize Bodily Responses Schachter’s cognitive attribution model (1962) - Emotional labels (e.g., anger, fear, joy) are attributed to relatively nonspecific feelings of physiological arousal - Emotional experiences result from our interpretation of our physiological arousal and context (current social, physical, and psychological situation, including other’s emotions) Figure 15.2 Cognition Plays a Role in the Experience of Emotion (Part 1) - Participants were injected with epinephrine (unknowingly) causing respiration, increased blood pressure and heart rate - Participants interacted with a happy or angry confederate - Participants’ emotional experiences depended on how the confederates were acting > Emotional interpretation of physiological arousal depends on the emotions of others Figure 15.6 Basic Emotions Eight basic emotions (medium level) that come in four pairs of opposites: Joy/sadness Affection/disgust Anger/fear Expectation/surprise Figure 15.8 Cultural Differences in Recognizing Facial Expressions of Emotion People from isolated nonliterate groups less likely agree with literate people’s judgments of surprise and disgust How Many Emotions Do We Experience? Facial feedback hypothesis: sensory feedback from our facial expressions can affect our mood, (supporting the James-Lange theory) Manipulating facial expressions can alter a person’s mood > putting on a happy, cheerful expression can make you feel better How Many Emotions Do We Experience? Impairment of facial expressions: - observed in Parkinson’s disease, schizophrenia, and Bell’s palsy (partial facial paralysis causes by a virus) - may affect subjective experience of emotions - may affect social interactions Individuals using Botox report experiencing less intense emotions MacLean’s limbic system (1949) limbic = limbus = border Group of brain regions involved in emotion including subcortical (thalamus, hypothalamus, amygdala, hippocampus) and cortical (prefrontal cortex, cingulate cortex) areas Higher-order thinking Emotions Ongoing debate on including new areas such as the septum and insular cortex There is no agreement what areas belong to the limbic system There is no unifying theory of the emotional brain Survival Do Distinct Brain Circuits Mediate Emotions? Anxiety disorders - Patients show fear responses in safe environments - Symptoms are a result of the fear system (mostly amygdala) breaking loose of the cortical controls (mostly prefrontal cortex) Fear learning requires the association between environmental cues and danger: Fear conditioning Fear conditioning studied in the lab: A neutral stimulus (e.g., tone) is repeatedly paired with an unpleasant experience (e.g. shock), causing the subject to act fearful in response to the neutral stimulus Figure 15.15 The Circuitry of Fear (Part 1) 1 day later Left: Hearing a tone does not increase blood pressure or freezing behavior Middle: Day 1 = Conditioning: Tone is paired with a shock, which causes increases in blood pressure and freezing behavior Right: Day 2 = Testing: Tone alone causes increases in blood pressure and freezing Figure 15.15 The Circuitry of Fear (Part 2) Fear-inducing stimulus reaches the thalamus Thalamus to amygdala > mediates fast behavioral response Thalamus to cortex/hippocampus to amygdala > allows cognitive appraisal of fear-inducing stimulus, which may result in correcting behavioral response Amygdala: essential for fear recognition Adolphs et al., Nature 1994 Impaired recognition of emotion in facial expressions following bilateral damage to the human amygdala Control Patient SM SM: bilateral amygdala lesions red to control subjects (), SM () fails to recognize fear from facial exp  Amygdala: essential to direct attention to emotional cues Adolphs et al., Nature 2005 A mechanism for impaired fear recognition after amygdala damage was instructed to fixate on the eyes when viewing facial express SM has now a normalized accuracy to recognize fear expressions Damage to the amygdala impairs attention and exploration strat 16 Psychopathology: Biological Basis of Behavioral Disorders Figure 16.1 Prevalence of Serious Mental Illness among U.S. Adults Prevalence of mental illness depends on sex and age Mental illness occurs in every racial group Schizophrenia Is the Major Neurobiological Challenge in Psychiatry Schizophrenia Affects approx. 1% of the population Neurodevelopmental disorder (childhood-onset or adolescent-onset) Key symptom includes psychosis (loss of contact with reality), which may be associated with - dissociative thinking (impaired logical thought) - hallucinations (seeing/hearing things that aren’t there) - delusions (false beliefs about what is taking place or who one is) - changes in affect (emotion) Table 16.2 Symptoms of Schizophrenia Figure 16.4 Eye Tracking in Patients with Schizophrenia versus Controls People with schizophrenia have difficulty making smooth- pursuit movements with their eyes Eyes of people with schizophrenia move in jerks and fits rather than smoothly tracking the moving object as most people’s eyes do Schizophrenia Is the Major Neurobiological Challenge in Psychiatry Risk factors to develop schizophrenia Genetic (>100 genes involved; COMT gene involved in dopamine metabolism; DISC1 involved in synaptic plasticity) Environmental (stress; immigration; living in cities) Developmental (low birth weight, impaired motor coordination) Epigenetic (Paternal age) Schizophrenia Is the Major Neurobiological Challenge in Psychiatry More structural changes in schizophrenia - Hippocampus is smaller in size and hippocampal pyramidal neurons have disorganized arrangement > occurs during early brain development - Amygdala is smaller in size > may affect emotion - Corpus callosum is thicker with altered function - Frontal lobes show loss of gray matter and show reduced metabolic activity > Hypofrontality hypothesis suggests that schizophrenia may be caused by underactivation of the frontal lobes Figure 16.8 Cellular Disarray of the Hippocampus in Chronic Schizophrenia (A) The hippocampus is shown in green (B-C) Further enlargements of the hippocampus (D) The hippocampus consists of the dentate gyrus and three cornu ammonis subregions (CA1, CA2, CA3). (E) Pyramidal cells are found in the CA1 and are disorganized in patients with schizophrenia Schizophrenia Is the Major Neurobiological Challenge in Psychiatry Treatments for schizophrenia Brain surgery - Lobotomies (detached the frontal lobes from the rest of the brain) in the 1930s - Psychosurgery today, but is still very rare, is a last resort, and involves small lesions Drug treatment - Antipsychotics (e.g., haloperidol, clozapine), since the 1950s(!), block dopamine D2 receptors, primarily manage/control psychosis Cognitive behavioral therapy, to manage psychosis Schizophrenia Is the Major Neurobiological Challenge in Psychiatry Dopamine hypothesis of schizophrenia: Schizophrenia results from excess in dopamine function Pros: (1) Amphetamines enhance dopamine function and can induce psychosis, (2) Dopamine is important for cognitive function Cons: (1) Antipsychotics block D2 receptors immediately, but reduction of symptoms takes time (2) Not all patients respond to D2 receptor antagonists (3) Antipsychotics are ineffective in treating negative and cognitive symptoms Schizophrenia Is the Major Neurobiological Challenge in Psychiatry Phencyclidine (PCP, or angel dust) and ketamine at low doses - simulates almost all symptoms of schizophrenia - act as NMDA receptor antagonists and block glutamate actions at high doses - induces deep sleep - used as anesthetic (ketamine only) Role of OXT in social dysfunction in schizophrenia Keri et al., 2010 Goldman et al., 2008 Control Schizophrenia Oxytocin (pg/ml) Trust Neutral Schizophrenic patients: Schizophrenic patients: Fail to show an increase in Show greater accuracy of rating plasma OXT activation after facial emotions when trust-related interactions endogenous plasma OXT (sharing secrets with the levels were higher experimenter) Summary of OXT effects on social functioning in schizophrenia Two-week treatment with 24 IU OXT improved one aspect of theory of mind Two-week treatment with 24 IU OXT alleviated positive but not negative symptoms of schizophrenia > OXT may improve certain aspects of social cognition in certain individuals diagnosed with schizophrenia Mood Disorders Are a Major Psychiatric Category Treatments for depression: Cognitive behavioral therapy Drugs o Selective serotonin reuptake inhibitors o Monoamine oxidase inhibitors o Tricyclics o Ketamine (experimental) Electroconvulsive therapy (rare) Deep brain stimulation (experimental) Figure 16.23 The Treadmill of Depression Cognitive behavioral therapy aims to break the negative cycle by identifying thought distortions and maladaptive behaviors and focusing on action-based coping strategies Mood Disorders Are a Major Psychiatric Category Monoamine hypothesis of depression Based on accidental discovery of antidepressant effect of iproniazid (MAO inhibitor) in 1957 > Intended for the treatment of tuberculosis, but it elevated mood in patients with tuberculosis and in depressed patients w/o tuberculosis Monoamine oxidase (MAO) degrades monoamines (serotonin, norepinephrine, dopamine) > Suggests deficiency in monoamine function in depression  Serotonin neurotransmission Wong et al. (2005) Case history: the discovery of fluoxetine hydrochloride (Prozac). Nat Rev Drug Discov 4:764-74.  Monoamine Hypothesis of Depression normal brain depressed brain antidepressants Normal brain: 5-HT in synaptic cleft binds postsynaptic receptors and is recycled after reuptake by presynapstic 5-HT transporters Fewer monoamines in depressed brain cause insufficient monoamine signaling Antidepressants block 5-HT transporters to enhance 5-HT availability in synaptic cleft  Monoamine Hypothesis of Depression Support for this hypothesis 1. Monoamine-based antidepressant drugs successful in reducing depressive symptoms 2. Low levels of the 5-HT metabolite 5-HIAA in cerebrospinal fluid of depressed patients 3. Reduced concentrations of 5-HT and 5-HIAA in postmortem brain tissue of depressed patients 4. Depletion of 5-HT (tryptophan-free diet) worsens depressive state  Monoamine Hypothesis of Depression Problems with the monoamine hypothesis 1. Antidepressants work within minutes: > fast inhibition of re-uptake 5-HT/NA > fast increase in 5-HT/NA synaptic concentrations However: Therapeutic efficacy takes several weeks 2. Other drugs that inhibit 5-HT/NA re-uptake (e.g. cocaine) are not effective antidepressants 3. 5-HT/NA depletion in healthy individuals does not induce depression 4. Antidepressants do not elevate mood in healthy individuals Mood Disorders Are a Major Psychiatric Category Stress hormone dysregulation hypothesis of depression > High levels of glucocorticoids may cause depression Based on: - Hypercortisolemia (high levels of cortisol) > normalized by successful SSRI treatment, which could explain delayed therapeutic efficacy! - Resistance to glucocorticoid feedback inhibition - Adrenal and Pituitary hypertrophy - Increased cerebrospinal fluid CRH levels - Increase in CRH neurons in hypothalamus and amygdala - Cushing’s syndrome is induced by very high levels of glucocorticoids, and patients often show depression  Dexamethasone suppression test Used in clinic to evaluate HPA axis in depression > Important biomarker to monitor clinical course How does it work? Dexamethasone = synthetic glucocorticoid that activates glucocorticoid receptors (GR) in the periphery (dexamethasone cannot cross the blood- brain-barrier) Dexamethasone suppresses cortisol release via GR-mediated negative feedback at the level of the pituitary There Are Several Types of Anxiety Disorders Treatment of anxiety disorders: Cognitive behavioral therapy Drugs - SSRI’s - Serotonin receptor agonists (e.g., Buspirone) - Benzodiazepines (e.g,. Valium and Xanax) bind to GABA receptors and enhance GABA’s inhibitory actions by increasing the flow of Cl– ions into cells - Propranolol inhibits the actions of norepinephrine, being investigated as potential treatment of PTSD, phobias, and performance anxiety There Are Several Types of Anxiety Disorders Posttraumatic stress disorder (PTSD) also called combat fatigue, war neurosis, or shell shock, but can develop after any traumatic experience associated with - mental or physical distress to trauma-related cues - unpleasant memories (flashbacks), nightmares - memory changes, including amnesia - structural and functional changes in the brain, especially the prefrontal cortex, hippocampus, and amygdala > impaired ability to show fear extinction  Fear extinction in PTSD patients Bleichert et al., 2007 Skin conductance Negative valence of Shock expectancy conditioned stimulus PTSD Trauma exposed Non-trauma exposed PTSD:  skin conductance than non-trauma exposed >  fear response persistent negative evaluations of CS during extinction > resistance to extinction of cues associated with negative experience  US expectancy during habituation and during There Are Several Types of Anxiety Disorders Persistent fear memories in PTSD may be a failure to show fear extinction in a safe environment Signals from the prefrontal cortex to the amygdala normally suppress fear in a safe environment Prefrontal cortex signal to amygdala may lose effectiveness in suppressing fear in PTSD patients > Hypoactive prefrontal cortex > Hyperactive amygdala 17 Learning and Memory 17 Learning and Memory Learning is the process of acquiring new information. Memory is the result of learning. It is......the ability to store and retrieve information.... a change in behavior caused by experience.... RECONSTRUCTIVE 17 Learning and Memory Amnesia is where there is an impairment in memory. Retrograde amnesia is the loss of memories formed before onset of amnesia, and is not uncommon after brain trauma. Anterograde amnesia is the inability to form new memories after onset of a disorder. 17 Learning and Memory Patient H.M., Henry Molaison, suffered from severe epilepsy. Because his seizures began in the temporal lobes, a decision was made to remove the anterior medial temporal lobes on both sides. H.M.’s surgery removed the amygdala, hippocampus, and some cortex. 17 Learning and Memory H.M. was able to improve his motor skills with practice, but could not remember performing them. 17 There Are Several Kinds of Learning and Memory Two kinds of memory: Declarative memory: “what”, explicit  Facts and information acquired through learning that can be stated or described.  Things we are aware that are learned. Nondeclarative (procedural) memory: “how”, implicit  Shown by performance rather than conscious recollection.  Things we learn by doing. 17 There Are Several Kinds of Learning and Memory Two subtypes of declarative memory Semantic memory: generalized memory Episodic memory: detailed autobiographical memory Patient K.C. could not retrieve personal (episodic) memory due to damage to the cortex and severe shrinkage of the hippocampus and parahippocampal cortex; his semantic memory was good. 17 There Are Several Kinds of Learning and Memory Five subtypes of nondeclarative memory Skill learning: learning to perform a task requiring motor coordination Priming: a change in stimulus processing due to prior exposure to the stimulus Associative learning: the association of two stimuli or of a stimulus and a response Spatial memory: learning about the locations of objects and places in the environment Nonassociative learning: a change in response following repeated exposure 17 There Are Several Kinds of Learning and Memory Two subtypes of associative learning Operant Conditioning: Response-Outcome Classical Conditioning: Stimulus-Outcome 17 There Are Several Kinds of Learning and Memory Early work indicated that animals form a cognitive map: an understanding of relative spatial organization. Place cells in the hippocampus become active when an animal is in or moving toward a particular location. Grid cells in the entorhinal cortex fire when an animal crosses intersection points of an abstract grid. Arrival at the perimeter of a spatial map is signaled by firing of entorhinal border cells. 2014 Nobel Prize: "for their discoveries of cells that constitute a positioning system in the brain" 17 Successive Processes Capture, Store, and Retrieve Information in the Brain Memories can last a variety of durations: Sensory buffer: store sensory impressions that only last a few seconds. Short-term memories (STMs)/working memory: last up to 30 seconds or throughout rehearsal. Long-term memories (LTMs): lasts days to years 17 Successive Processes Capture, Store, and Retrieve Information in the Brain A functional memory system incorporates three aspects: Encoding: sensory information > STM Consolidation: STM > LTM Retrieval: LTM info is used, memory becomes plastic 17 Successive Processes Capture, Store, and Retrieve Information in the Brain Mechanisms differ for STM and LTM storage. Primacy effect: better recall for items at the beginning of a list (LTM). Recency effect: better recall for items at the end of a list (STM). 17 Successive Processes Capture, Store, and Retrieve Information in the Brain The medial temporal lobe is crucial for the conversion of STM > LTM, but LTMs are not stored there. Permanent storage, after consolidation, tends to occur in the regions where info was first processed. 17 Successive Processes Capture, Store, and Retrieve Information in the Brain The hippocampus is crucial for the conversion of STM > LTM, but LTMs are stored in cortex. Fig 13.39: Physiology of Behavior, 11th ed, Carlson 17 Memory Storage Requires Physical Changes in the Brain Changes in the amount of neurotransmitter released. Changes in neurotransmitter-receptor interactions (e.g, size of synaptic membranes, number of receptors on the synaptic membrane). 17 Memory Storage Requires Physical Changes in the Brain Changes in the rate of termination of transmitter signaling (e.g., reuptake or enzymatic degradation). Inputs from other neurons may modulate neurotransmitter release. 17 Memory Storage Requires Physical Changes in the Brain New synapses could form or be eliminated with training. Training might also lead to synaptic reorganization. 17 Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits Donald Hebb (1949) proposed that when two neurons are repeatedly activated together, their synaptic connection becomes stronger. “Cells that fire together wire together” Cell assemblies—ensembles of neurons— linked via Hebbian synapses could store memory traces. 17 Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits When researchers applied a tetanus (brief high-frequency burst of electrical stimuli) to the hippocampus, the response of postsynaptic neurons increased. Long-term potentiation (LTP): a stable and enduring increase in the effectiveness of synapses. LTP is critically dependent on NMDA glutamate receptors. 17 Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits When large levels of glutamate are released, the postsynaptic membrane depolarizes and the Mg2+ plug is released from the NMDA receptor. This allows for an influx of Ca2+, which results in activation of CaMKII which has several important effects on AMPA receptors. 17 Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits CAMKII causes: More AMPA receptors to be inserted into the active synapse. Increased conductance of Na+ and K+ ions in membrane- bound AMPA receptors. ​ he end result is the synapse T is more sensitive to the effects of glutamate.​ This is important for the early stages of LTP. ​ 17 Synaptic Plasticity Can Be Measured in Simple Hippocampal Circuits Influx of Ca2+ via active NMDA receptors also results in activation of CREB. CREB binds to DNA promoter regions and changes the transcription rate of genes.  receptors, kinases, actin/actin- associated genes Inhibition of protein synthesis prevents longer-lasting LTP and the formation of LTM. 17 The Cutting Edge: Artificial Activation of an Engram Reactivating the neurons that were active during fear conditioning in context B caused mice to freeze in context A, even though they were in a different, “safe”, context. Turning the light off again caused the animals to resume activity, indicating that they remained unafraid of context A.