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PSY209 Exam 4
| Question | Answer |
|---|---|
| emotion | a subjective mental state accompanied by distinctive behaviors, feelings, and involuntary physiological changes; complex evaluative (positive or negative) reaction of the nervous system in response to internal (bodily, biochemical) or external stimuli |
| fundamental emotions | fear, anger, surprise, disgust, happiness, sadness |
| what are emotional states caused by? | the activation of the autonomic nervous system |
| sympathetic nervous system | "fight or flight" system; activates the body for action |
| parasympathetic nervous system | prepares the body to relax and recuperate |
| why are emotions important? | evolutionary adaptations and central to social communication |
| evolutionary adaptations | enhance an organism's ability to experience and evaluate its environment |
| central to social communication | enhance an organism's ability to interact and communicate with others in appropriate ways |
| what are emotions associated with? | overt behaviors (crying, laughter), motivational states (approach, avoidance), and physiological arousal (increased heart beat, perspiration) |
| what is emotional dysregulation central to? | psychopathologies |
| folk psychology | emotions cause autonomic responses (like stomach churning); feeling triggers autonomic reaction |
| James-Lange theory (1884) | bodily changes cause the emotions we feel, emotions differ due to different physiological responses; autonomic reaction triggers feeling |
| Cannon-Bard theory (1927) | emotions are independent of physiological responses and help deal with a changing environment; simultaneous feeling and autonomic reaction |
| 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 |
| what does the emotional interpretation of physiological arousal depend on? | the emotion of others |
| what affects the emotion we experience? | cognitive analysis of the situation |
| what increases emotion intensity? | sympathetic activation |
| polygraph test (lie detector) | records multiple physiological measures; based on the assumption that lying produces emotional and physiological responses |
| What is a drawback to a polygraph? | physiological responses of an anxious person can be similar to those of a liar |
| what is an alternative to a polygraph? | brain imaging |
| what does a polygraph measure? | sympathetic activation (increase in respiration, skin conductance and heart rate) which are signs of arousal |
| What does a PET (positron emission topography) scan reveal in a lying patient? | selective activation of prefrontal cortex |
| what did Charles Darwin determine about emotions? | expressions and emotions come from a common ancestor, animal emotions are homologues to human emotions, and a limited set of fundamental emotions are present across species and cultures |
| eight basic emotions that come in four pairs of opposites | joy/sadness, affection/disgust, anger/fear, and expectation/surprise |
| facial feedback hypothesis | sensory feedback from our facial expressions can affect our mood (supports the James-Lange theory) |
| impairment of facial expressions | observed in Parkinson's disease, schizophrenia, and Bell's palsy (partial facial paralysis caused 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) | group of brain regions involved in emotion including subcortical and cortical areas |
| subcortical area | thalamus, hypothalamus, amygdala, hippocampus |
| cortical area | prefrontal cortex, cingulate cortex |
| what are the areas debated to be part of MacLean's limbic system? | the septum and insular cortex |
| what brain regions produce pleasure? | septum and nucleus accumbens |
| what brain regions produce fear? | amygdala |
| what brain areas respond to brain self-stimulation? | those that receive dopamine projections from the ventral tegmental area through the medial forebrain bundle |
| 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) |
| what does fear learning require? | the association between environmental cues and danger (fear conditioning) |
| how is 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 |
| what does fear-inducing stimulus reach? | 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 |
| what nuclei does the amygdala consist of? | lateral nucleus and central nucleus |
| lateral nucleus | role in fear learning and projects to central nucleus |
| central nucleus | mediates response |
| Patient SM | had bilateral amygdala lesions; compared to control subjects, fails to recognize fear from facial expressions and fails to fixate on the eyes when viewing facial expressions |
| what happens after SM is instructed to fixate on the eyes when viewing facial expressions? | they have a normalized accuracy to recognize fear expressions |
| what does damage to the amygdala impair? | attention and exploration and strategies |
| different emotions activate.... | .....different brain regions |
| same brain region may be active in..... | .....different emotions |
| each emotion involves.... | ....differential patterns of activation across a network of brain regions involved in emotion |
| what typical regions are activated? | the amygdala, insula, caudate, putamen, cingulate cortex, prefrontal cortex |
| physiological responses | can precede the awareness of feeling an emotion (conform James-Lange theory) |
| What does prevalence of mental illness depend on? | sex and age |
| What is the prevalence of serious mental illness in the overall population? | 4% |
| What percentage of the population is affected by schizophrenia? | approximately 1% |
| psychosis | loss of contact with reality; can be characterized by dissociative thinking, hallucinations, delusions, and changes in affect |
| What does prevalence of mental illness depend on? | sex and age |
| hallucinations | seeing/hearing things that aren't there |
| delusions | false beliefs about what is taking place or who one is |
| changes in affect | changes in emotion |
| key symptom of schizophrenia | psychosis |
| positive symptoms of schizophrenia | hallucinations, delusions, and excited motor behavior |
| positive symptoms | abnormal behaviors that are gained |
| negative symptoms of schizophrenia | slow thought and speech, emotional and social withdrawal, and blunted affect or emotional expression |
| negative symptoms | result of lost functions |
| cognitive symptoms of schizophrenia | memory problems, poor attention span, difficulty making plans, reduced decision-making capacity, poor social cognition, abnormal movement patterns |
| cognitive symptoms | problems with processing and acting on external information |
| what do people with schizophrenia have difficulty with? | making smooth-pursuit movements with their eyes |
| what is the accuracy of eye movements on a mathematical model for people with schizophrenia? | 96% |
| What is the prevalence of serious mental illness in the overall population? | 4% |
| genetic risk factors for schizophrenia | over 100 genes involved; COMT gene involved in dopamine metabolism; DISC1 involved in synaptic plasticity |
| What percentage of the population is affected by schizophrenia? | approximately 1% |
| environmental risk factors for schizophrenia | stress; immigration; living in cities |
| psychosis | loss of contact with reality; can be characterized by dissociative thinking, hallucinations, delusions, and changes in affect |
| developmental risk factors for schizophrenia | low birth weight, impaired motor coordination |
| 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 | changes in emotion |
| DISC1 gene | disrupted in schizophrenia 1; mutations associated with schizophrenia, bipolar disorder, and depression; transgenic mice with mutated DISC1 develop enlarged lateral ventricles; role in synaptic plasticity |
| key symptom of schizophrenia | psychosis |
| what is the DISC1 gene supposed to do? | neuronal proliferation, neuronal migration, regulators of key signaling pathway, spine regulation, synapse maintenance |
| positive symptoms of schizophrenia | hallucinations, delusions, and excited motor behavior |
| how does living in a city affect schizophrenia risk? | living in larger cities makes it twice as likely for someone to develop schizophrenia; children who move to the city later in life have a lower risk than children who move to the city earlier in life |
| positive symptoms | abnormal behaviors that are gained |
| environmental stress and genetic susceptibility | may lead to the development of a schizophrenic disorder (with spectrum disorders, schizotypy, and schizophrenia from mild to severe) |
| negative symptoms of schizophrenia | slow thought and speech, emotional and social withdrawal, and blunted affect or emotional expression |
| why do children who are born to older fathers have a higher risk of schizophrenia? | DNA damage in sperm is higher in older men |
| negative symptoms | result of lost functions |
| cognitive symptoms of schizophrenia | memory problems, poor attention span, difficulty making plans, reduced decision-making capacity, poor social cognition, abnormal movement patterns |
| cognitive symptoms | problems with processing and acting on external information |
| what do people with schizophrenia have difficulty with? | making smooth-pursuit movements with their eyes |
| what is the accuracy of eye movements on a mathematical model for people with schizophrenia? | 96% |
| what are the risk factors for developing schizophrenia? | genetic, environmental, developmental, epigenetic |
| genetic risk factors for schizophrenia | over 100 genes involved; COMT gene involved in dopamine metabolism; DISC1 involved in synaptic plasticity |
| environmental risk factors for schizophrenia | stress; immigration; living in cities |
| developmental risk factors for schizophrenia | low birth weight, impaired motor coordination |
| epigenetic risk factors for schizophrenia | paternal age |
| DISC1 gene | disrupted in schizophrenia 1; mutations associated with schizophrenia, bipolar disorder, and depression; transgenic mice with mutated DISC1 develop enlarged lateral ventricles; role in synaptic plasticity |
| what is the DISC1 gene supposed to do? | neuronal proliferation, neuronal migration, regulators of key signaling pathway, spine regulation, synapse maintenance |
| how does living in a city affect schizophrenia risk? | living in larger cities makes it twice as likely for someone to develop schizophrenia; children who move to the city later in life have a lower risk than children who move to the city earlier in life |
| environmental stress and genetic susceptibility | may lead to the development of a schizophrenic disorder (with spectrum disorders, schizotypy, and schizophrenia from mild to severe) |
| why do children who are born to older fathers have a higher risk of schizophrenia? | DNA damage in sperm is higher in older men |
| what structural changes do the brains of schizophrenic patients show? | cerebral ventricles can be enlarged, which predict poorer response to drug treatment |
| how is the hippocampus different in a schizophrenic patient? | smaller in size and hippocampal pyramidal neurons have disorganized arrangement (occurs during early brain development) |
| how is the amygdala different in a schizophrenic patient? | smaller in size and may affect emotion |
| how is the corpus callosum different in a schizophrenic patient? | thicker with altered function |
| how is the frontal lobe different in a schizophrenic patient? | loss of gray matter and reduced metabolic activity |
| hypofrontality hypothesis | schizophrenia may be caused by under activation of the frontal lobes |
| what does the hippocampus consist of? | dentate gyrus and three Cornu ammonis subregions (CA1, CA2, CA3) |
| pyramidal cells | found in the CA1 and are disorganized in patients with schizophrenia |
| what happens to the brains of adolescents with schizophrenia? | they lose gray matter at a faster rate |
| what do schizophrenia patients show on PET scans during tasks that require frontal lobe activation and at rest? | less frontal cortex activation than control participants |
| treatments for schizophrenia | brain surgery, drug treatment, cognitive behavioral therapy |
| lobotomies | detached the frontal lobes from the rest of the brain in the 1930s |
| psychosurgery | still very rare, used as a last result, involves small lesions |
| antipsychotics | e.g. haloperidol, clozapine; since the 1950s, block dopamine D2 receptors, primarily manage/control psychosis |
| cognitive behavioral therapy | to manage psychosis |
| dopamine hypothesis of schizophrenia | schizophrenia results from excess in dopamine function |
| support of dopamine hypothesis of schizophrenia | amphetamines enhance dopamine function and can induce psychosis; dopamine is important for cognitive function |
| refutation of dopamine hypothesis of schizophrenia | antipsychotics block D2 receptors immediately, but reduction of symptoms takes time; not all patients respond to D2 receptor antagonists; antipsychotics are ineffective in treating negative and cognitive symptoms |
| 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 |
| phencyclidine (PCP, or angel dust) and ketamine at high doses | induces deep sleep; used as anesthetic (ketamine only) |
| glutamate hypothesis of schizophrenia | schizophrenia is caused by reduced glutamate function |
| support of glutamate hypothesis of schizophrenia | optimal glutamate function is requiring for frontal lobe and hippocampal function; glutamate can affect dopamine function which has been implicated in schizophrenia |
| refutation of glutamate hypothesis of schizophrenia | glutamate medication is not effective |
| what is the role of oxytocin (OXT) in social dysfunction in schizophrenia? | oxytocin is important for optimal social functioning and schizophrenic patients show social dysfunction; schizophrenic patients have lower plasma OXT activation; schizophrenic patients show inverse correlation of OXT and prosocial behaviors |
| oxytocin and schizophrenia hypothesis | diminished OXT activity could contribute to the social dysfunction in schizophrenia |
| what have studies found about using oxytocin as a treatment for schizophrenia? | more than 100 published studies; OXT improves some social cognition aspects, negative symptoms, higher order social cognition, empathic accuracy, social cognition, social perception, verbal memory, emotion recognition, and some aspects of theory of mind |
| after trust-related interactions, schizophrenic patients.... | .....fail to show an increase in plasma OXT activation |
| when endogenous plasma OXT levels were higher, schizophrenic patients.... | .....show greater accuracy of rating facial emotions |
| effects of OXT on theory of mind and social perception in schizophrenics | schizophrenia patients received twice daily 24 IU intranasal OXT or placebo for 2 weeks; social cognition measures and psychiatric measures |
| social cognition measures | Bruene Theory of Mind Picture Stories Task, Trustworthiness Task |
| psychiatric measures | positive and negative symptom scale (PANSS), paranoia scale |
| Bruene Theory of Mind Picture Stories Task | assessment of the ability to infer somebody else's mental state using a computerized cartoon sequencing task and a questionnaire |
| Bruene Theory of Mind Picture Stories Task Intention Questions | answer can be positive (cooperation) or negative (deception) |
| Bruene Theory of Mind Picture Stories Task Beliefs Questions | answer can be false beliefs (incorrect assumptions) or true beliefs |
| positive and negative symptom scale (PANSS) | medical scale used for measuring symptom severity of patients with schizophrenia |
| OXT induced improvement in.... | ....accurate identification of second order (involves modeling what person A thinks person B thinks) false beliefs in the Bruene task; all PANSS scores except for PANSS negative; paranoia scale |
| summary of OXT effects on social functioning in schizophrenia | 2 week treatment with 24 IU OXT improved 1 aspect of theory of mind and alleviated positive but not negative symptoms of schizophrenia; OXT may improve certain aspects of social cognition in certain individuals diagnosed with schizophrenia |
| depression | characterized by persistent anhedonia, sadness, emptiness, hopelessness, helplessness, and worthlessness; associated with low energy and appetite, difficulty concentrating, and restless agitation |
| anhedonia | inability to experience pleasure |
| what percentage of the population will be affected by depression in their lifetime? | 16% |
| what percentage of the population is affected by depression each year? | 6.6% |
| what can depression cause? | loss of work, substance abuse, and suicide |
| major depression | unipolar depression; characterized by a combination of symptoms that are disabling |
| dysthymia | chronic depression; lowered mood but not as severe as in major depression |
| bipolar depression | manic depression; periods of clinical depression alternated by extreme elation or mania |
| atypical depression | overeating, oversleeping, fatigue, mood changes in response to events |
| psychotic depression | major depression along with loss of touch with reality (psychosis) |
| postpartum depression | depression in women after giving birth that outlasts the baby blues |
| premenstrual dysphoric disorder | severe form of premenstrual syndrome with depression symptoms |
| seasonal affective disorder | depression that occurs each year at the same time (mostly in winter) |
| treatments for depression | cognitive behavioral therapy, drugs, electroconvulsive therapy (rare), deep brain stimulation (experimental) |
| what drugs are used to treat depression? | selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, tricyclics, and ketamine (experimental) |
| what is cognitive behavioral therapy's purpose? | aims to break the negative cycle by identifying thought distortions and maladaptive behaviors and focusing on action-based coping strategies. |
| the treadmill of depression | thoughts (negative): there is no point in trying; mood (low): feel guilty, discouraged, inadequate, and worthless; behavior (reduced): become less active, avoid people and situations |
| monamine hypothesis of depression | based on accidental discovery of antidepressant effect of iproniazid (MAO inhibitor) in 1957; mood disorders are caused by a deficiency in serotonin and/or norepinephrine at functionally important receptor sites in the brain |
| iproniazid | intended for the treatment of tuberculosis, but it elevated mood in patients with tuberculosis and in depressed patients without tuberculosis |
| monamine oxidase (MAO) | degrades monoamines (serotonin, norepinephrine, dopamine); suggests deficiency in monoamine function in depression |
| fluoxetine (Prozac) | first selective serotonin reuptake inhibitor (SSRI) in 1987 |
| venlafaxine (Effexor) | first serotonin-norepinephrine-reuptake inhibitor (SNRI) in 1994 |
| what do antidepressants block? | re-uptake of monoamines which increases in extracellular monoamine concentrations |
| tryptophan hydroxylase (TH) | catalyses the conversion of tryptophan (TRYP) to 5-hydroxytryptophan (5-HTP) |
| aromatic aminoacid decarboxylase (AADC) | catalyses the conversion of 5-HTP to 5-hydroxytryptamine (5-HT, serotonin) |
| 5-HT is taken up into.... | .....storage vesicles; the presynaptic 5-HT terminals by the 5-HT transporter |
| 5-HT is released.... | .....from storage vesicles into the synaptic space |
| 5-HT can activate..... | .....subtypes of 5-HT receptor families (1,2,3,4,5,6, and 7), which couple with their respective system of signal transduction inside the postsynaptic neuron |
| within the presynaptic 5-HT terminals, 5-HT would either be taken up by.... | .....the storage vesicles or degraded by monoamine oxidase (MAO) |
| 5-HT activates..... | ......the presynaptic somatodendritic 5-HT 1A auto receptor which can be blocked by selective 5-HT 1A antagonists |
| what inhibits the 5-HT transporter? | selective serotonin-reuptake inhibitors (SSRIs) including fluoxetine |
| normal brain | 5-HT in synaptic cleft binds postsynaptic receptors and is recycled after reuptake by presynaptic 5-HT transporters |
| what causes insufficient monamine signaling in the depressed brain? | fewer monamines |
| antidepressants | block 5-HT transporters to enhance 5-HT availability in synaptic cleft |
| support for monamine hypothesis of depression | monamine-based antidepressant drugs successful in reducing depressive symptoms; low levels of the 5-HT metabolite 5-HIAA in cerebrospinal fluid of depressed patients reduced concentrations of 5-HT and 5-HIAA in postmortem brain tissue of depressed patient |
| what does depletion of 5-HT (tryptophan-free diet) do? | worsens depressive state |
| problems with monoamine hypothesis of depression | antidepressants work within minutes, other drugs that inhibit 5-HT/NA re-uptake (cocaine) are not effective antidepressants, 5-HT/NA depletion in healthy individuals does not induce depression, antidepressants do not elevate mood in healthy individuals |
| why do antidepressants work within minutes? | fast inhibition of re-uptake 5-HT/NA and fast increase in 5-HT/NA synaptic concentrations, however therapeutic efficacy takes several weeks |
| stress hormone dysregulation hypothesis of depression | high levels of glucocorticoids may cause depression |
| what is the stress hormone dysregulation hypothesis of depression based on? | hypercortisolemia, 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 |
| hypercortisolemia | high levels of cortisol; normalized by successful SSRI treatment, could explain delayed therapeutic efficacy |
| what is Cushing's syndrome induced by? | very high levels of glucocorticoids, and patients often show depression |
| corticotropin-releasing hormone (CRH) | produced in the hypothalamus stimulates ACTH release from the anterior pituitary into the blood stream |
| ACTH | stimulates glucocorticoid production and release from the adrenal glands into the blood stream |
| glucocorticoids | mediate their effects on the periphery and the brain and also mediate a negative feedback via the brain and pituitary |
| what do depressed patients as a group show? | much more variation in serum cortisol levels compared with psychiatric and healthy controls |
| what do depressed patients show on average compared with psychiatric and healthy controls? | higher serum cortisol levels |
| dexamethasone | synthetic glucocorticoid which activates glucocorticoid receptors (GR) in the periphery (dexamethasone cannot cross the blood-brain-barrier); blocks the release of cortisol by GR-mediated negative feedback at the level of the pituitary |
| in depressed patients, dexamethasone.... | .....is less effective in blocking cortisol release |
| dexamethasone suppression test | used in clinic to evaluate HPA axis in depression, important biomarker to monitor clinical course |
| what happens when dexamethasone binds to GR in the anterior pituitary? | inhibits the release of ACTH, less ACTH leads to less release of cortisol |
| deep brain stimulation | achieved by an implanted battery powered neurostimulator placed subcutaneously in the chest area; safe, adjustable (brain activity can be continuously adjusted for each patient), and reversible (electrodes can be completely removed if necessary) |
| first study of deep brain stimulation in BA25 | patients with depression show hyper metabolism in BA25, BA25 involved in modulating negative mood states, decrease in BA25 activity linked to clinical response to antidepressant treatments |
| goal of deep brain stimulation | reduce BA25 hyperactivity by chronic stimulation of white matter tracts adjacent to BA25 |
| result of deep brain stimulation | 4/6 patients showed sustained remission of depression, reduced blood flow in BA25 and in limbic and cortical areas |
| anxiety disorders | generalized anxiety disorder, social anxiety disorder, post traumatic stress disorder, panic disorder, phobic disorder |
| generalized anxiety disorder | persistent, excessive anxiety, and worry |
| social anxiety disorder | fear and avoidance of negative public scrutiny, public embarrassment, humiliation, or social interaction |
| post traumatic stress disorder (PTSD) | anxiety disorder that results from a traumatic experience; also called combat fatigue, war neurosis, or shell shock, but can develop after any traumatic experience |
| panic disorder | recurrent attacks of intense fearfulness |
| phobic disorder | irrational fears centered on an object, activity, or situation that a person avoids |
| treatment of anxiety disorders | cognitive behavioral therapy and drugs |
| what drugs treat anxiety disorders? | SSRIs, serotonin receptor agonists (e.g. Buspirone), benzodiazepines (e.g. Valium and Xanax), propranolol |
| benzodiazepines | 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 |
| what is PTSD 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, impaired ability to show fear extinction |
| what parts of the brain are changed by PTSD? | prefrontal cortex, hippocampus, and amygdala |
| fear acquisition | a neutral stimulus (tone) is paired with an unpleasant stimulus (shock); increase in fear response |
| fear extinction | with repeated tone-alone presentations, freezing decreases; the tone itself no longer elicits fear |
| what are persistent fear memories in PTSD caused by? | a failure to show fear extinction in a safe environment |
| what do signals from the prefrontal cortex to the amygdala normally do? | suppress fear in a safe environment |
| why does the prefrontal cortex signal to the amygdala lose effectiveness in suppressing fear in PTSD patients? | hypoactive prefrontal cortex or hyperactive amygdala |
| what does it mean for the prefrontal cortex to amygdala pathway to be impaired? | allows enhanced emotional responses mediated by the amygdala when being exposed to trauma-related emotional stimuli |
| what is the amygdala central to? | traumatic memory formation, but there is a network of other systems (stress, sensory, cognitive) that play a role in further strengthening of long-lasting fearful reactions |
| acute neurochemical responses activated by original trauma | locus coeruleus (norepinephrine), ventral tegmental area (dopamine), endogenous opioids, corticotropin-releasing hormone |
| what do reciprocal interactions facilitate? | encoding and retrieval of traumatic memories |
| successive processes | capture, store, and retrieve information in the brain |
| what does memory storage require? | physical changes in the brain |
| what do invertebrate nervous systems show? | plasticity |
| how can synaptic plasticity be measured? | in simple hippocampal circuits |
| learning | the process of acquiring new information |
| memory | the result of learning; the ability to store and retrieve information and a change in behavior caused by experience; reconstructive |
| amnesia | where there is an impairment in memory |
| retrograde amnesia | the loss of memories formed before onset of amnesia, and is not uncommon after brain trauma |
| anterograde amnesia | the inability to form new memories after onset of a disorder |
| what can disrupt memories? | storage failure (the amnesia is permanent) or retrieval failure (the amnesia is temporary, maybe) |
| Patient H.M. (Henry Molaison) | suffered from severe epilepsy, seizures would begin in temporal lobes so the anterior medial temporal lobes on both sides of his brain were removed which removed the amygdala, hippocampus, and some cortex; had severe anterograde amnesia |
| H.M. was able to improve.... | .......his motor skills with practice, but could not remember performing them |
| what can H.M. teach us about learning and memory? | the medial temporal lobes are involved in memory, short-term and long-term memory are separate, memory can exist that cannot be recalled |
| two kinds of memory | declarative and non declarative |
| declarative memory | "what," explicit; facts and information acquired through learning that can be stated or described; things we are aware that we learned |
| non declarative (procedural) memory | "how," implicit; shown by performance rather than conscious recollection; things we learn by doing |
| what do patients with more focal damage to the hippocampus confirm? | its role in declarative memory |
| two subtypes of declarative memory | semantic and episodic |
| 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 |
| five subtypes of nondeclarative memory | skill learning, priming, associative learning, spatial memory, and non associative learning |
| 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 |
| non associative learning | a change in response following repeated exposure |
| two subtypes of associative learning | operant conditioning and classical conditioning |
| operant conditioning | response-outcome |
| classical conditioning | stimulus-outcome |
| 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 |
| entorhinal border cells | when fired, signal the arrival at the perimeter of a spatial map |
| 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 |
| three aspects of a functional memory system | encoding, consolidation, retrieval |
| encoding | sensory information to STM |
| consolidation | STM to LTM |
| retrieval | LTM info is used, memory becomes plastic |
| 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) |
| where does permanent storage occur? | in the regions where information was first processed |
| pattern completion | a subset of the original experience can activate the memory for the entire experience |
| pattern separation | establish different indices for each memory |
| what happens when lidocaine is injected in the hippocampus one day after learning a task? | no memory of the task |
| what happens when lidocaine is injected in the hippocampus thirty days after learning a task? | good memory of the task |
| what happens when lidocaine is injected in the cortex one day after learning a task? | good memory |
| what happens when lidocaine is injected in the cortex thirty days after learning a task? | no memory |
| Charles Sherrington (1897) | speculated that alterations in synapses were the basis for learning |
| memory storage requires.... | changes in the amount of neurotransmitter released |
| changes in neurotransmitter-receptor interactions | size of synaptic membranes, number of receptors on the synaptic membrane |
| changes in the rate of termination of transmitter signaling | reuptake or enzymatic degradation |
| inputs from other neurons.... | ....may modulate neurotransmitter release |
| new synapses | could form or be eliminated with training |
| synaptic reorganization | caused by training |
| what can varied experiences and learning cause? | robust neural changes such as heavier, thicker cortex, more dendritic branches, with more dendritic spines, suggesting more synapses |
| what did Donald Hebb (1949) propose? | when two neurons are repeatedly activated together, their synaptic connection becomes stronger |
| cell assemblies | ensembles of neurons linked via Hebbian synapses |
| Hebbian synapses | could store memory traces |
| what happened when researchers applied a tetanus to the hippocampus? | the response of postsynaptic neurons increased |
| tetanus | brief high-frequency burst of electrical stimuli |
| long-term potentiation (LTP) | a stable and enduring increase in the effectiveness of synapses |
| what is LTP critically dependent on? | NMDA glutamate receptors |
| during normal, low-level activity.... | .....the release of glutamate only activates AMPA receptors |
| NMDA receptor | inactive because of block by Mg2+ ion |
| AMPA receptor when activated | depolarizes cell |
| when large levels of glutamate are released.... | .....the postsynaptic membrane depolarizes and the Mg2+ plug is released from the NMDA receptor |
| an influx of Ca2+, which results in.... | .....activation of CaMKII which has several important effects on AMPA receptors |
| Induction of LTP | enhances subsequent transmitter release > AMPA receptors added to postsynaptic membrane > retrograde messengers; no arachidonic acid, and others; increased Ca2+ concentration leads to activation of protein kinases |
| CAMKII causes | more AMPA receptors to be inserted into the active synapse, increased conductance of Na+ and K+ ions in membrane-bound AMPA receptors; end result is the synapse is more sensitive to the effects of glutamate |
| influx of Ca2+ via active NMDA receptors.... | ....also results in activation of CREB |
| what does CREB bind to? | DNA promoter regions and changes the transcription rate of genes; receptors, kinases, actin/actin-associated genes |
| what does inhibition of protein synthesis prevent? | longer-lasting LTP and the formation of LTM |
| channelrhodopsin (ChR) | a protein that excites cells when exposed to blue light |
| for mice with blue light in the dentate gyrus region of the hippocampus and produced ChR when neurons were active..... | .....special diet blocked production of ChR, removed from diet so ChR produced, and special diet blocked further production of ChR |
| 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 |
| The James-Lange theory of emotion argues that each emotion is produced by | perception of a unique bodily change provoked by a stimulus |
| the Cannon-Bard theory of emotions would predict that people with severe spinal cord injuries would | experience the same emotions that others do |
| evidence that two different emotions are associated with approximately the same autonomic profile supports | Schachter's cognitive attribution model |
| which individual is likely to feel happiest after receiving a poor mark on an exam? | Drew, who forces a grin and tries to bear it |
| patients with Bell's palsy | lose control over some facial muscles, resulting in distorted displays of emotion |
| neural circuitry of fear | thalamus, lateral amygdala, central amygdala, brainstem |
| what strategy would be helpful for humans to improve their ability to recognize fear in facial expressions of other people? | instruct them to direct their attention to the eyes |
| which of the following is a positive symptom of schizophrenia? | hallucinations |
| which of the following is a negative symptom of schizophrenia? | social withdrawal |
| what is not considered a risk factor for schizophrenia? | maternal age |
| a principal effect of antipsychotic drugs is | postsynaptic blocking of dopamine receptors |
| a patient who is given antipsychotics to control the symptoms of schizophrenia may | develop Parkinson's disease-like symptoms |
| which of the following statements is true? | plasma OXT levels in schizophrenic patients correlate positively with their ability to identify emotions in facial expressions |
| a MAO inhibitor______while an SSRI________ | prevents degradation of serotonin; prevents re-uptake of serotonin |
| according to the monamine hypothesis, depression is caused by | decreased synaptic activity of norepinephrine and serotonin |
| which features of the hypothalamic-pituitary-adrenal axis may be observed in depression? | excessive high levels of cortisol and decreased negative feedback |
| in healthy individuals, dexamethasone treatment | reduces the release of ACTH |
| SSRIs affect | serotonin |
| benzodiazepines affect | GABA |
| propranolol affects | norepinephrine |
| SNRIs affect | serotonin and norepinephrine |
| fear extinction in PTSD may be reduced because | the prefrontal cortex fails to inhibit the amygdala |
| bilateral damage to the anterior medial temporal lobes may lead to severe | anterograde amnesia and impairments in declarative memories |
| in instrumental/operant conditioning, an association is formed between an animal's behavior and | its consequences/outcome |
| successive process for memory formation | 1. encoding 2. consolidation 3. storage 4. retrieval |
| learning can result in | the addition of synapses, the removal of synapses, change in amount of neurotransmitter released, and two more things |
| according to Hebb's notion of cell assemblies, information can be stored by groups of neurons that are | activated simultaneously or in close succession |
| in the formation of LTP, the entry of Ca2+ into the neuron activates______which______protein synthesis | NMDA receptors; activates |
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