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Cognitive experience; affective reaction; a physiological response (sympathetic nervous system, locus coeruleus, which produces NE, which causes heightened arousal and vigilance; also produces epinephrine from adrenal glands which causes physical symptoms of fight or flight) Cultural universality; similarities between humans and animals Somatic nervous system activation (facial nerve 7) Physiological feedback may not be necessary, but adds intensity; patients with spinal cord injury have full range of emotions Conscious appraisal may not be necessary, but allows us to plan and execute a response |
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James-Lange theory of emotion |
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The theory that a stimulus produces a physiological response which produces an emotion; you react before you feel an emotion |
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Cannon-Bard theory of emotion |
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The theory that a stimulus elicits an emotion which produces a physiological response |
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Schachter-Singer theory of emotion |
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The theory that a person needs to experience physiological arousal and cognitively attribute the arousal to an appropriate stimulus Gave two groups of participants an injection of epinephrine; activates the sympathetic nervous system; first group thought they were getting a multivitamin, and were not warned about side effects; second group thought they were getting a multivitamin with lots of side effects; participants are then put in a room with an angry or euphoric confederate; the no-side effect group reported the same emotion as the confederate; the side-effect group did not report or demonstrate any change in emotion based on the confederate; group that was not aware of side effects had to attribute those feelings to something, and figured they were having the same response as the confederate, whereas the side-effect-aware group was already expecting it |
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Vascular theory of emotion |
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A theory based on changes in bloodflow through blood vessels in your face rushing out of the face (cavernous sinus), the brain cools just a little and causes happy emotions; blood pooling in the face causes slight warming of the brain and negative emotions |
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Right hemisphere- understanding and expression Both hemispheres- feeling emotion; right - negative, left - positive |
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Emotions that evoke a fight or flight response; anger, fear Amygdala- particularly the central and basolateral nucleus- is most important part of the brain for this Amygdala may activate the basal ganglia, which organizes and initiates behavior, and the periaqueductal gray; prefrontal cortex is vital to the expression of emotions |
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If you put an electrode in this part of the brain and stimulate it, it will produce fear, anxiety, and rage Damage to this area produces difficulty identifying fear and anger Imaging has shown that this area is more active when viewing expressions of fear Contains GABA and endorphin receptors Lateral nucleus Central nucleus and basolateral nucleus- most involved in negative emotions |
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Caused by damage to the amygdala Tend to be low in fear and aggression; eat too much or inappropriate objects; hyper-sexuality regarding inappropriate objects |
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Damage to this part of the brain causes increased rage Phineas Gage |
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Higher levels of this reduces aggression |
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Norepinephrine and dopamine |
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More of these substances increases aggression |
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More of this hormone can increase aggression |
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Overactivation of our flight response Increasing GABA (with benzodiazepines/anxiolytics) decreases this; enhance the effects of GABA at receptors to open channels for longer periods of time |
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Too much fight response Includes dementia, brain injury, mental retardation, epilepsy, Huntington's disease, intermittent explosive disorder |
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Intermittent explosive disorder |
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Rage not associated with another disorder Too little serotonin, too much norepinephrine Treated with SSRIs (increase serotonin) and beta blockers (decrease norepinephrine) |
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Generalized anxiety disorder |
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Uncontrolled worry Free-floating chronic (>6 months) worry Physical symptoms include (autonomic underarousal) headaches, muscle tension, stomach aches, irritability |
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Intense fear of an object or situation; greater response than the threat merits Specific- e.g. spiders, heights, flying Social- fear of social situations and being scrutinized Agoraphobia- fear of spaces or areas that are difficult to escape from; e.g. elevators, crowds |
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Repeated and >1 hour/day immersion in obsessions, compulsions, or both (typically comorbid) Obsessions can include contamination, sex, aggression, religion, symmetry Compulsions can include checking, patterns, counting, arranging, washing, repeating, hoarding |
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Treatments for anxiety disorders |
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Beta blockers, benzodiazepines (except for OCD), SSRIs (works best for OCD) |
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Happiness, joy, euphoria Uses the mesolimbic dopamine pathway; medial forebrain bundle (MFB- bundle of axons between the VTA and nucleus accumbens that release dopamine) Ventral tagmental (VTA) > nucleus accumbens > prefrontal cortex Activation of any of these parts causes pleasure |
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How all of the different neurotransmitter systems work together Excitatory neurons in the hypothalamus release serotonin > serotonin causes endorphins to be released in the VTA > endorphins inhibit the release of GABA (dopamine neurons in the VTA are disinhibited) > can release dopamine into the nucleus accumbens |
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Reward deficiency syndrome |
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A disorder characterized by decreased activity in the nucleus accumbens and hippocampus Abnormal A1 allele- inactive dopamine receptor (D2) Dysphoria; cravings for substances that increase dopamine Often abuse drugs, alcohol, sex, food, etc. |
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Drugs that produce alterations in consciousness, emotion, and behavior LSD, cocaine, heroine, amphetamines, marijuana, alcohol, nicotine, caffeine |
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A maladaptive use of a substance that is not considered dependent |
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When a person becomes physically and psychologically dependent on a substance Physically dependent when they develop tolerance and withdrawal Psychologically dependent when cravings occur Addictive substances activate the reward cascade; also triggered by positive emotions Addicts can have low levels of D2 receptor activity - A1 allele Treat withdrawal symptoms and psychological dependence; pharmacological treatments such as methadone |
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Delirium tremens (the DTs) |
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Definition
A condition experienced during very severe withdrawal from alcohol Extreme shaking, disorientation, confusion, terrifying visual hallucinations, memory problems |
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Hedonic homeostatic dysregulation model |
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Definition
A model of addiction Withdrawal (negative affect; dopamine\/, opioids\/, stress^ - negative reinforcer) > preoccupation (anticipation; stress hormones^, opioids^, dopamine^) > binge (intoxication; dopamine^, opioids^ - positive reinforcer) >back to withdrawal and the cycle continues The more and more an individual goes through the withdrawal-negative affect phase- dopamine levels drop more; more drug must be consumed to produce the desired rewarding effects |
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A negative experience accompanied by characteristic emotional, behavioral, biochemical, and physiological responses Can be caused by catastrophic events (natural disasters, war, terrorist attacks), major life events (divorce, moving, having a baby, getting fired, death in the family), and hassles (minor life events that are not catastrophic but very annoying; traffic, chores, broken items) Can be studied by exposing subjects to stressful stimuli or using subjects who are already stressed; can measure depression, hopelessness, anxiety, anger, heart rate, blood pressure, or corticosteroids Paraventricular nucleus receives info from various areas of the nervous system about stressors (NST (major organs like gut), tegmentum and reticular formation (somatosensory input), periaqueductal gray (pain), locus coeruleus (detects changes in heart rate, blood pressure), limbic system (BNST)) > triggers a cascade of events that results in stress hormones being released |
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Occurs infrequently and for a short period of time |
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Occurs repeatedly or for a long period of time |
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Initiated by locus coeruleus-- activates the sympathetic nervous system; increases heart rate, blood flow, and respiration Also initiated by the paraventricular nucleus-- Hypothalamic-Pituitary-Adrenal (HPA) Axis-- hypothalamus releases corticotropic-releasing hormone (CRH > anterior pituitary releases adrenocorticotropic hormone (ACTH) > stimulates the adrenal glands to produce glucocorticoids (corticosterone in animals, cortisol in humans) > elevates blood glucose levels to improve brain and body function > negative feedback loop Interactions between LC and HPA axis: positive feedback loop; reciprocal excitation |
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Suppresses our immune systems-- the body's defense against malignant cells or invading pathogens Easy development of colds |
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Effects of chronic stress |
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On the LC: repeated exposure to a stressor causes habituation (decrease in release of NE from the LC); add a novel stressor to the situation causes sensitization (increase in release of NE) On the HPA axis: negative feedback loop doesn't work as effectively; increased levels of glucocorticoids in the body and brain Long-term, glucocorticoids can cause regression and loss of dendritic spines in the hippocampus-- learning and memory impairments; increases amount of calcium entering the cells (increases amount of neurotransmitter released); too much calcium can be excitotoxic to neurons and cause cell death; neurons in the hippocampus are particularly vulnerable-- becomes significantly smaller in PTSD patients and people who have experienced long-term abuse |
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Hypothalamic-Pituitary-Adrenal (HPA) |
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Hypothalamus releases corticotropic-releasing hormone (CRH) Anterior pituitary releases adrenocorticotropic hormone (ACTH) Stimulates the adrenal glands to produce glucocorticoids |
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Exposure to at least one tragic event Flashbacks-- reoccurring distressing memories of the event Hyperactivity of the LC |
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Major depressive disorder |
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Lingering depressed mood or diminished interest in pleasurable activities Eating disturbances, sleep disturbances, lack of energy or restlessness, difficulty concentrating, feelings of hopelessness and worthlessness Hyperactivity of the HPA axis; excess of CRH and cortisol released; down-regulation of CRH receptors in the brain Norepinephrine hypothesis: deficit of NE in critical areas of the brain; tricyclic antidepressants and MAOIs are effective treatments; increase NE levels in the synapse; may cause structural changes in neurons that were damaged by chronic stress Low levels of thyroid hormone in ~30% of depressed patients Low levels of estrogen (menopause, after childbirth, PMS) Melatonin dysfunction (less time in SWS; altered distributions of REM) |
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A change in an organism's behavior or thought as a result of experience |
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A change in behavior that has taken place with conscious awareness |
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Acquisition of behavior for which we have no conscious awareness; conditioning, forming habits, habituation |
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Change in magnitude of response to environmental events Habituation and sensitization |
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Connection between two elements or events Classical conditioning and operant conditioning |
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The process of responding less strongly over time to repeated stimuli Repeated stimuli > sensory neuron releases less neurotransmitter > motor neuron... Normally, there are 1300 axon terminals on sensory neurons; decreases to 800 axon terminals |
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Responding more strongly over time Dangerous or irritating stimuli Normally, there are 1300 axon terminals on sensory neurons; increases to 2800 axon terminals Serotonin increase |
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Father of operant conditioning Law of effect: if a stimulus elicited behavior results in a reward, the stimulus is more likely to elicit behavior in the future |
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Substantial loss of memory and other cognitive abilities in the elderly Impairments in memory, attention, language, problem solving Beyond normal aging Most common form is Alzheimer's Disease |
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Disorientation, cognitive impairments in language and declarative memory Plaques: clumps of amyloid protein that cluster among axon terminals and interfere with neural transmission Tangles: abnormal accumulation of tau protein inside neurons; associated with death of neurons Loss of synapses beyond that of normal aging Degeneration of acetylcholine neurons Cell death in the hippocampus and cerebral cortex Enlarged/exaggerated ventricles and sulci |
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Fertilized egg Blastocyst for a while, then folds to become the neural tube |
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Balls of cells Trophoblast cells- placenta Embryonic stem cells |
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2nd - 8th week of prenatal development, during which limbs, facial features, and major organs of the body take form |
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Period of prenatal development from the 9th week until birth All major organs have formed |
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5 Stages of brain development |
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Cell proliferation: begins 4 weeks after fertilization; neurons are forming at a rate of 250,000 cells a minute Cell migration: begins about 6 weeks after fertilization; glial cells and proteins direct migration; neurons born first migrate closest to the neural tube Cell differentiation: 7-8 weeks after fertilization; immature neurons begin to change shape Axonal and dendritic growth: begins about 10 weeks after fertilization and continues long after birth; neurotrophins aid in dendritic and axonal growth- helps neurons form synaptic connections; nerve growth factor was the first discovered Cell death: primarily happens after birth; apoptosis- programmed cell death; glutamate is the main neurotransmitter |
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Chemical insults to the developing brain |
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When the embryo/fetus is exposed to poisons or toxins consumed by the mother Fetal Alcohol Syndrome, |
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Behavioral and cognitive deficits Interferes with cell migration |
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Physical insults to the developing brain |
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Radiation- affects cell migration Physical damage to the brain Diseases and malnutrition; syphilis- deafness and absence of a vestibular system Genetic abnormalities- Down's Syndrome (3 chromosomes for #21); Holoprosencephaly (only one cerebral hemisphere develops; can also be born with only one eye; cause is unknown) |
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Brain damage produced by trauma |
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Concussion: a blow to the head that results in bruising of the brain Contusion: head is jarred with such force that the brain becomes shifted in the skull and badly bruised Cerebral laceration: tearing of outer surface of the brain (bullet, pieces of skull, blood clots) |
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Brain damage produced by disease |
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Meningitis: bacterial infection of the meninges (protective layers around the brain) Syphilis: in its final stage gets into the brain; extensive damage to frontal lobes; cognitive and emotional impairments Viral encephalitis: virus transmitted by mosquitoes; 50% of people with VE will die AIDS-related dementia: damage to cerebral cortex; emotional blunting, cognitive difficulty, apathy, confusion; 35% of AIDS patients |
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Memory impairments due to alcohol abuse |
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Korsakoff's syndrome: caused by a deficiency in vitamin thiamine (B1); anterograde amnesia; severe damage to mamillary bodies |
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Brain function develops normally when damage occurs in infancy; critical period |
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Structural changes in the brain after injury |
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The brain is plastic; neurogenesis (growth of neurons) happens beyond childhood, especially in the hippocampus Waste removal by glial cells Regrowth of axons |
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Severe mental disorders in which thinking is disturbed and the affected person is not well oriented for person, time, and place Can be reversible or irreversible |
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"Split mind"; disorganization of associations leading to disconnected thoughts, words, and emotions Loss of contact with reality Inability to function normally in daily life 1.5% prevalence during lifetime; 2.5 million Americans in a given year; equally split between genders, though males have earlier onset (18-25 for males, 25-35 for females; this is because the prefrontal cortex is not done developing until this age Positive symptoms: delusions, hallucinations, disorganized speech ("word salad"), motor disturbances Negative symptoms: social and emotional engagement, appropriate emotional response, normal cognition or affect Cognitive deficits: organization and reorganization of thoughts, attention deficits Increased size of ventricles and sulci in the brain (takes up room where frontal lobes would be); decreased activation and size of the amygdala, hippocampus, and frontal lobe A majority of patients and 45% of their relatives show abnormal saccades in smooth pursuit tasks (eye movements) Dopamine hypothesis: positive symptoms caused by an excess of dopamine (drugs that inhibit dopamine help control symptoms, drugs that promote dopamine can produce symptoms, like cocaine and amphetamines); increase in density of DA receptors; overactivity of DA in the mesolimbic system (midbrain, amygdala, hippocampus- emotion and reward) and nigrostriatal pathway (substantia nigra to basal ganglia- movement); underactivity of dopamine in the mesocortical pathway (midbrain to cortex- cognition; not affected by antipsychotic drugs) Glutamate hypothesis: PCP produces symptoms similar to schizophrenia by blocking NMDA glutamate receptor; schizophrenia symptoms may be related to abnormalities with glutamate, because overactivity of DA blocks glutamate release Prenatal exposure to virus or trauma or other brain development disruptions may be a cause of schizophrenia Diathesis-stress model: genetics, biological processes, and perinatal insults can all predispose a person to develop schizophrenia; major life stressors can trigger the disorder if good coping skills are not present |
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Consistent, abnormal patterns of behavior that progress for a long period of time Cognitive difficulties, emotional impairments, impulsive behaviors, disruptions in interpersonal functioning Schizophrenic spectrum disorders: genetically related to schizophrenia |
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Schizoid personality disorder |
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Genetically related to schizophrenia; social detachment and flat affect; no positive symptoms |
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Borderline personality disorder |
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Condition marked by extreme instability in mood, identity, and impulse control Self-destructive behaviors, manipulation of others, intense feelings of abandonment when alone Serotonin, dopamine, and opiate systems implicated in this disorder |
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Antisocial personality disorder |
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Criminal behavior; impulsivity/aggression; disregard for safety and wellbeing of others; lack of remorse |
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Nucleus accumbens, hippocampus, amygdala, septum, and olfactory bulb Parts of the prefrontal cortex, cingulate gyrus, hypothalamus, thalamus, and midbrain |
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When mood is altered in a way that affects daily life More profound than "feeling blue" or "feeling hyper"; more long-lasting, consistent, and interfering Unipolar disorders: major depressive, dysthymic, postpartum depression, seasonal affective Bipolar disorders: bipolar I, bipolar II, cyclothymia |
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If an axon of a presynaptic neuron is active while the postsynaptic neuron is firing, the synapse between them will be strengthened "Neurons that fire together wire together" |
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Long-term potentiation (LTP) |
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Definition
An increase in readiness for the post-synaptic neuron to fire following repeated stimulation by the presynaptic neuron Is relatively long-lasting Occurs in areas of the brain involved in memory (hippocampus, amygdala, cortex, and cerebellum) Glutamate: 2 receptor types: NMDA (Magnesium block) and Non-NMDA (AMPA) 1. Magnesium block removed from NMDA receptor 2. Calcium released into the post-synaptic neuron activate protein kinases 3. Nitric Oxide released from the post-synaptic side crosses the synapse and increases release of glutamate presynaptically 4. # of glutamate receptors increases Induces spine growth, spine number, and perforation and formation of MSB |
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Limited amounts of info are stored briefly 7 pieces of info at once |
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Large amounts of info is stored indefinitely |
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The process by which short-term memories are transferred to long-term memories |
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Temporary register for information while it is being used Different working memory sites: object identification, spatial location, verbal information Central executive system: coordinates the different working memory systems; prefrontal cortex & anterior cingulate cortex |
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Declarative memory (explicit) |
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Conscious retention of facts and events Episodic: memory for events in one’s own life (right hemisphere) Semantic: memory for general knowledge (left hemisphere) |
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Non-declarative memory (implicit) |
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Unconscious memory for learned behaviors, habits, skills, and classical conditioning Involves the cerebellum and corticostriatal pathway |
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An improvement in the ability to recognize particular stimuli following previous exposure to similar stimuli |
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Effects of emotion on memory |
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Norepinephrine and cortisol are released when you are emotionally aroused; they activate the amygdala which enhances hippocampal activity (increases consolidation) Also increases glucose availability in the brain |
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Inability to encode new memories from our experiences Can be caused by damage to the hippocampus |
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Loss of memories from our past |
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Condition marked by a history of at least one manic episode (dramatically elevated mood, decreased need for sleep, increased energy, impaired judgment) Low levels of Serotonin & NE; high levels of dopamine Treatments: lithium alone, lithium + anti-depressants |
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