Physio Psych Final

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  1. 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.
  2. Operational Definition of Fear
    • Changes in heart rate, blood pressure, blood flow, pupil size, respiration
    • vocalizations, analgesia, potentiation of reflexes
    • autonomic nervous system
  3. 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
  4. Cannon-Bard Theory
    • Experience precedes response
    • See a bear --> experience fear --> run
  5. Limbic System
    • Involved with negative emotions
    • 10% of brain
  6. 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
  7. 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
  8. 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
  9. Hypothalamus
    • "master gland"
    • releasing hormones (RH) released into circulatory system which connects the hypothalamus and the pituitary gland
  10. Pituitary Gland
    • Connected to to hypothalamus by HP portal system (blood system)
    • releases tropic hormones into the blood to affect distant cells
  11. 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)
  12. 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.
  13. 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
  14. 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
  15. Anxiety
    • behaviors similar to fear, but without a discrete stimulus
    • PTSD, OCD, generalized anxiety disorder
  16. 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
  17. Anxiolytic Drugs: Benzodiazepines
    • Newer, safer
    • Valium, Xanax
    • date-rape drugs: rohypnol
    • sedating: drowsiness, confusion, dizziness, visual disturbances
    • can be lethal when mixed with alcohol
  18. 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
  19. Cross-Tolerance
    • tolerance to one drug --> tolerance to related drugs
    • Barbiturates, benzodiazepines, and alcohol all show cross-tolerance
  20. Aggression
    • Low serotonin, high aggression
    • measure actual serotonin in animals, but metabolite in humans
  21. 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
  22. Donald Hebb
    • Organization of Behavior (1943)
    • father of behavioral neuroscience
    • learning/behavior can be studied as biological processes
  23. 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
  24. Engram
    • the physical representation of a memory in the brain
    • hypothetical construct
  25. Consolidation
    the process by which short-term memories become long-term memories
  26. Declarative Memory
    • Memories for facts, dates, faces
    • Have you seen this task before?
    • Explicit memory: conscious recollection
  27. Procedural Memory
    • Memories for procedures or skills
    • how to do something
    • Can you perform this task?
    • Implicit memory: unconscious performance
  28. Retrograde Amnesia
    inability to remember events that occurred prior to the brain trauma
  29. Anterograde Amnesia
    inability to remember events that occurred after the brain trauma - cannot form new memories
  30. 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
  31. 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
  32. 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
  33. Plaques and Tangles
    • Plaques: amyloid deposits
    • Tangles: accumulation of tau protein (MAP)
    • in Alzheimer's, tau detaches so axons cannot function
    • affects neuronal communication
  34. Treatment for Alzheimer's
    • ACh agonists
    • AChE inhibitors
    • Nerve Growth Factor
    • Estrogen-Replacement Therapy
    • Marijuana
  35. 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)
  36. Hebbian Synapse
    A synapse that increases its effectiveness because of simultaneous activity in pre- and post-synaptic neurons
  37. 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
  38. 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)
  39. 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
  40. 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
  41. LTP Brain Areas
    • Hippocampus
    • Amygdala
    • Cerebellum
    • Prefrontal Cortex
    • areas known to be involved in learning/memory
  42. In Vitro vs. In Vivo
    • In vitro - in glass
    • in vivo - in a living organism
  43. 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
  44. 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)
  45. What does your brain need?
    • Glucose - energy
    • Amino acids - precursors to neurotransmitters and hormones
    • Elements - zinc, iron, magnesium
    • Ions - communication; Na+, K+, Cl-, Ca++
  46. Digestion
    • Saliva and chewing
    • Esophagus - moves food to stomach
    • Stomach - gastric enzymes, mechanical breakdown
    • Intestines - absorption of nutrients, water
  47. Energy
    • Glucose - simple sugar, immediate energy
    • Glycogen - short-term storage/reserve
    • Fat (lipids) - longer-term storage
  48. Insulin
    • Converts glucose to glycogen
    • glucose transporters bring glucose into cells
    • lack of insulin --> diabetes
  49. 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
  50. 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
  51. 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
  52. 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
  53. Hypothalamus and Eating
    • Paraventricular nucleus (PVN) responds to NPY
    • Arcuate nucleus is sensitive to hunger and satiety signals
  54. 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
  55. 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.
  56. Treatment for Obesity
    • Exercise
    • Target reward pathway (eating = drug addiction)
    • gastric bypass surgery
  57. Binge Eating
    • activates DA and opiate reward systems, like drug addiction
    • can be reduced with morphine
  58. Binging and Purging
    • associated with low serotonin (5-HT) levels
    • SSRIs can treat binge eating
  59. Anorexia Nervosa
    • altered 5-HT and DA systems
    • Comorbid with depression, anxiety, and OCD
  60. 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)
  61. 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
  62. 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
  63. 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)
  64. Treatment for Bipolar Disorder
    • Conventional antidepressants can make it worse - rapid cycling or trigger a switch
    • Mood-stabilizers like lithium
    • MRI scans
  65. 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
  66. Glutamate Theory of Schizophrenia
    • PCP blocks NMDA-receptor ion channel
    • PCP intoxication mimics positive and negative symptoms
  67. Current Theory of Schizophrenia
    • Overactivity at DA receptors and underactivity at NMDA receptors
    • Treatment involves neuroleptics (DA antagonists) and NMDA agonists together
  68. Tardive Dyskinesia
    • Parkinson-like movement disorder
    • characterized by involuntary movements
    • side effect of neuroleptics
    • discontinuing drug treatment does not reverse effects
  69. Dopamine Pathways
    • Nigrostriatal: movement
    • Mesolimbic: reward, pleasure
    • Mesocortical: complex thought, decision making
  70. Atypical Neuroleptics
    • Clozapine
    • selective D4 receptor antagonist
    • does not affect movement dopamine pathway, so no tardive dyskinesia
  71. 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
  72. Left Hemisphere
    • language, mathematical, analytical, elemental, sequential, logical
    • complex language
    • controls right side of body
    • sees the right visual field
  73. 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)
  74. Split Brain
    • Corpus callosum severed
    • Roger Sperry
  75. 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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Author:
 alcollins
ID:
 302134
Filename:
 Physio Psych Final
Updated:
2015-05-10 20:58:58
Tags:
Physiological Psychology
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Physio Psych Final Review
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