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Operational Definition
- applicable to both humans and nonhuman animals, this is a change in observable, measurable behaviors without a subjective self-report
- smiling, frowning, etc.
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Operational Definition of Fear
- Changes in heart rate, blood pressure, blood flow, pupil size, respiration
- vocalizations, analgesia, potentiation of reflexes
- autonomic nervous system
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James-Lange Theory
- Response precedes experience
- See a bear --> run --> experience fear
- If you activate muscles needed to produce a Duchenne smile, the person reports being happier
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Cannon-Bard Theory
- Experience precedes response
- See a bear --> experience fear --> run
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Limbic System
- Involved with negative emotions
- 10% of brain
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Stress
Activates sympathetic nervous system
- quick onset, short-term response
- release of norepinephrine
- increases heart rate, blood pressure, and respiration
- Glycogen --> glucose
- more oxygen, more glucose --> body ready to mobilize
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Stress
HPA Axis
- Hormonal response
- Long response, slower onset
- Amygdala communicates with hypothalamus
- Hypothalamus releases corticotropin releasing hormone (CRH) into HP portal system --> pituitary release ACTH --> adrenal gland releases cortisol
- Negative Feedback: end-product CORT regulates release, and the hypothalamus has CORT receptors
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Endocrine System
- hormones
- chemicals that act at receptors on target cells to change their activity
- target cells far away by being released into the circulatory system
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Hypothalamus
- "master gland"
- releasing hormones (RH) released into circulatory system which connects the hypothalamus and the pituitary gland
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Pituitary Gland
- Connected to to hypothalamus by HP portal system (blood system)
- releases tropic hormones into the blood to affect distant cells
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Stress and Health
- increased risk of ulcers: bacterial, parasympathetic rebound (not stress, but after-effects that cause problems)
- CORT diverts energy from protein synthesis, which affects the immune system by lowering B, T, and killer cells
- High, persistent endorphin levels suppress immune system
- Too much CORT toxic to hippocampal cells (CORT activates hippocampus which turns off HPA axis, which decreases CORT release --> vicious cycle)
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Fear-Potentiated Startle
- Davis and colleagues
- 2 types of test trials
- "fear" - bigger response
- stimulus is usually a loud noise or bright light, response can include blinking, "jumping," etc.
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Fear Behavior and Brain Area
- Immobility or fight/flight --> PAG
- Changes in heart rate --> dorsal motor, Vagus (PNS)
- Changes in blood pressure --> lateral hypothalamus (SNS)
- Fear-potentiation of the startle reflex --> Pontine nuclei
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Urbach-Wiethe Disease
- rare, recessive gene
- bilateral calcification of the amygdala
- inability to express, identify with, or remember what fear is
- subjective experience of fear resides in the amygdala
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Anxiety
- behaviors similar to fear, but without a discrete stimulus
- PTSD, OCD, generalized anxiety disorder
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Anxiolytic Drugs: Barbiturates
- Sedative
- earliest class --> highly addictive
- high incidence of overdose
- tolerance --> effective dose becomes higher and approaches lethal dose
- death from respiratory depression
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Anxiolytic Drugs: Benzodiazepines
- Newer, safer
- Valium, Xanax
- date-rape drugs: rohypnol
- sedating: drowsiness, confusion, dizziness, visual disturbances
- can be lethal when mixed with alcohol
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Anxiolytic Drugs: Indirect GABA agonist
- inhibitory --> reduce amygdala activity
- bind to GABA receptors to facilitate GABA binding, so bonds longer and stronger
- increased GABA --> increased inhibition of amygdala
- no effect without GABA
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Cross-Tolerance
- tolerance to one drug --> tolerance to related drugs
- Barbiturates, benzodiazepines, and alcohol all show cross-tolerance
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Aggression
- Low serotonin, high aggression
- measure actual serotonin in animals, but metabolite in humans
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Learning/Memory
- Evolutionary adaptation to a nonstatic environment
- allows us to adapt to changing conditions
- relatively permanent change in behavior as a result of a specific prior experience
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Donald Hebb
- Organization of Behavior (1943)
- father of behavioral neuroscience
- learning/behavior can be studied as biological processes
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Karl Lashley
- Hypothesis: the engram is located in the cerebral cortex; if you can locate it, you can take it out
- Conclusions: Memory is stored diffusely in the brain, no localizable engram, all parts of the cortex play an equal role in memory storage
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Engram
- the physical representation of a memory in the brain
- hypothetical construct
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Consolidation
the process by which short-term memories become long-term memories
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Declarative Memory
- Memories for facts, dates, faces
- Have you seen this task before?
- Explicit memory: conscious recollection
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Procedural Memory
- Memories for procedures or skills
- how to do something
- Can you perform this task?
- Implicit memory: unconscious performance
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Retrograde Amnesia
inability to remember events that occurred prior to the brain trauma
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Anterograde Amnesia
inability to remember events that occurred after the brain trauma - cannot form new memories
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Modern Views on Memory
- Medial temporal lobe is important for some types of memory
- especially the hippocampus
- declarative, not procedural, memories
- consolidation of memories to long-term
- long-term declarative memories do not reside in the hippocampus
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Korsakoff's Syndrome
- seen in chronic alcoholics
- due to thiamine deficiency
- degeneration of mammillary bodies, which provide input to the hippocampus
- severe anterograde amnesia, declarative affected more than procedural
- late stages: retrograde amnesia
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Alzheimer's Disease
- definitive diagnosis at autopsy
- Chromosomes 21, 14, 1, and 19
- Memory loss linked to loss of ACh to hippocampus and in nucleus basalis
- ACh antagonists (scopolamine) interfere with memory
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Plaques and Tangles
- Plaques: amyloid deposits
- Tangles: accumulation of tau protein (MAP)
- in Alzheimer's, tau detaches so axons cannot function
- affects neuronal communication
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Treatment for Alzheimer's
- ACh agonists
- AChE inhibitors
- Nerve Growth Factor
- Estrogen-Replacement Therapy
- Marijuana
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Richard Thompson
- Eyeblink conditioning requires the cerebellum
- Engram in the lateral interpositus nucleus
- LIN receives information about the CS (tone) and the US (air puff)
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Hebbian Synapse
A synapse that increases its effectiveness because of simultaneous activity in pre- and post-synaptic neurons
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Long-Term Potentiation (LTP)
- Bliss and Lomo (1973)
- Form of synaptic plasticity
- a long lasting change (days or weeks) in the activity of a cell as a result of presynaptic tetanic stimulation
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Procedure for LTP
- Record from pyramidal neurons
- Baseline: Stimulate Schaffer collaterals with weak stimulus (record pyramidal cell response)
- Tetanic stimulation of Schaffer collaterals (experience)
- Test: present original weak stimulus to Schaffer collaterals (record pyramidal cell response)
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Molecular Mechanisms of LTP
- NMDA blocked by Mg++
- Activation of AMPA allows NA+ to enter cell, causes depolarization
- depolarization removes Mg++
- so glutamate is now able to bind to NMDA
- ion channels open
- Na+ and Ca++ move into the cell, K+ moves out
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AMPA-fication
- caused by Ca++ entry into the cell
- AMPA receptors more responsive to glutamate
- some NMDA receptors change into AMPA receptors
- Dendrites build more AMPA receptors
- When glutamate binds to AMPA, gets larger depolarization
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LTP Brain Areas
- Hippocampus
- Amygdala
- Cerebellum
- Prefrontal Cortex
- areas known to be involved in learning/memory
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In Vitro vs. In Vivo
- In vitro - in glass
- in vivo - in a living organism
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Pyramidal Neurons
- get input from Schaffer collaterals, exhibit experience-dependent changes in activity
- spines (sites of synaptic contact) grow and retract as a function of learning/experience
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Tri-Synaptic Circuit
- Perforant gyrus sends axon to dentate gyrus (synapse 1)
- dentate gyrus sends axons to area CA3 (synapse 2)
- CA3 sends axons (known as Schaffer collaterals) to an area CA1 (synapse 3 on pyramidal neurons)
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What does your brain need?
- Glucose - energy
- Amino acids - precursors to neurotransmitters and hormones
- Elements - zinc, iron, magnesium
- Ions - communication; Na+, K+, Cl-, Ca++
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Digestion
- Saliva and chewing
- Esophagus - moves food to stomach
- Stomach - gastric enzymes, mechanical breakdown
- Intestines - absorption of nutrients, water
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Energy
- Glucose - simple sugar, immediate energy
- Glycogen - short-term storage/reserve
- Fat (lipids) - longer-term storage
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Insulin
- Converts glucose to glycogen
- glucose transporters bring glucose into cells
- lack of insulin --> diabetes
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Stimulation of Insulin Release
- Cephalic phase: conditioned insulin release; sight, smell of food
- Digestive phase: food in stomach and intestines
- Absorptive phase: receptors in liver detect glucose in blood
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Set-Point Theories of Eating
- Eating is the result of an energy deficit
- Energy set-point is the optimal level
- After a meal, energy resources are high so we stop eating
- Later energy stores are low so we feel hungry
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Positive-Incentive Theories
- We are drawn to eat by the anticipated pleasure of eating
- Evolutionary pressures of unexpected food shortages cause us to take advantage of good food, when available
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Hormones/Peptides
- Leptin: hormone secreted by fat cells, more fat stored = more leptin secreted, leptin suppresses eating
- CCK: released by stomach; produce feelings of satiety
- Orexins: stimulate food intake; food deprivation increases orexin levels
- Ghrelin: released by cells in stomach; stimulates appetite; fasting --> increased ghrelin release, satiety --> decreased ghrelin release
- Galanin: controls fat intake, metabolism, and storage; increases fat consumption, particularly active at puberty
- Neuropeptide Y: increases intake of carbohydrates; promotes storage of excess carbs as body fat
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Hypothalamus and Eating
- Paraventricular nucleus (PVN) responds to NPY
- Arcuate nucleus is sensitive to hunger and satiety signals
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Serotonin and Eating
- decreases amount-per-meal ingested
- shift in preference away from fatty foods
- SSRIs can regulate eating patterns and is a treatment for some eating disorders
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Causes of Obesity
- Defective ob gene, so they make less leptin
- Prader-Willi Syndrome: 4-5x higher blood levels of ghrelin, so no decline after eating
- Hormonal disorders
- Behavioral: higher fat/sugar content, sedentary lifestyle, etc.
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Treatment for Obesity
- Exercise
- Target reward pathway (eating = drug addiction)
- gastric bypass surgery
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Binge Eating
- activates DA and opiate reward systems, like drug addiction
- can be reduced with morphine
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Binging and Purging
- associated with low serotonin (5-HT) levels
- SSRIs can treat binge eating
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Anorexia Nervosa
- altered 5-HT and DA systems
- Comorbid with depression, anxiety, and OCD
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Causes of Unipolar Depression
- Genetics
- Viruses: Borna, treatment - Amantadine, anti-viral
- Abnormal hemispheric dominance: low activity in left (positive emotions), and high activity in right (negative emotions)
- Hormonal: postpartum, menopause, problem with HP axis
- Stress
- Altered neurotransmitter activity (NE, DA, 5-HT)
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Antidepressant Drugs
- MAOIs: block MAO in presynaptic terminal, side effect - Cheese effect (tyramine)
- Tricyclics: blocks reuptake of monoamines, produces dysphoria in normals, side effectsL drowsiness, heart irregularities, dry mouth
- SSRIs: blocks reuptake of serotonin so it stays in the synapse longer
- SNRIs: blocks reuptake of serotonin and norepinephine
- Atypical: Wellbutrin, DA reuptake inhibitor, no effect on serotonin
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Monoamine Theory of Depression
- Developed from effectiveness of anti-depressant drugs
- Depression caused by low levels of serotonin, norepinephrine, and/or dopamine
- Problems with theory: inconsistent time-course effects, some drugs that increase catecholamines are not effective antidepressants (like cocaine and amphetamine), and monoamine metabolites do not differ a lot from normals
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5-HTT Gene and Depression
- Codes for serotonin transporter
- 2 alleles, long or short
- People with at least one short may be more susceptible to depression, because the amygdala is overactive (negative emotions)
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Treatment for Bipolar Disorder
- Conventional antidepressants can make it worse - rapid cycling or trigger a switch
- Mood-stabilizers like lithium
- MRI scans
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Dopamine Theory of Schizophrenia
- overactivity of DA
- Strengths: effective neuroleptics act at DA receptors, amphetamine causes greater DA release than in normals
- Weaknesses: inconsistent time-course of drug effects, schizos have the same DA metabolites as normals, neuroleptics affect positive symptoms not negative
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Glutamate Theory of Schizophrenia
- PCP blocks NMDA-receptor ion channel
- PCP intoxication mimics positive and negative symptoms
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Current Theory of Schizophrenia
- Overactivity at DA receptors and underactivity at NMDA receptors
- Treatment involves neuroleptics (DA antagonists) and NMDA agonists together
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Tardive Dyskinesia
- Parkinson-like movement disorder
- characterized by involuntary movements
- side effect of neuroleptics
- discontinuing drug treatment does not reverse effects
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Dopamine Pathways
- Nigrostriatal: movement
- Mesolimbic: reward, pleasure
- Mesocortical: complex thought, decision making
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Atypical Neuroleptics
- Clozapine
- selective D4 receptor antagonist
- does not affect movement dopamine pathway, so no tardive dyskinesia
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Right Hemisphere
- emotional, nonverbal communication, music perception/appreciation, creativity, holistic, spatial
- word recognition
- simple language
- controls left side of body
- sees the left visual field
- specialized for face recognition
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Left Hemisphere
- language, mathematical, analytical, elemental, sequential, logical
- complex language
- controls right side of body
- sees the right visual field
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Fiber Tracts connecting left and right hemispheres
- Anterior Commissure: connects anterior subcortical structures
- Hippocampal Commissure: connects left and right hippocampus
- Corpus Callosum: connects left and right hemispheres (cortex)
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Split Brain
- Corpus callosum severed
- Roger Sperry
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Mirror Neuron Theory
- cells responsible for imitation, empathy, modeling of behavior and emotions
- premotor cortex: mirror visual actions and activate to sounds related to actions (typing, paper ripping)
- somatosensory cortex
- parietal lobe
- anterior cingulate (limbic system): responds when experiencing an emotion or viewing another exhibiting an emotion
- temporal lobe: respond when watching someone speaking
- abnormal development of mirror neurons may cause autism
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