Intro to Psychological Science Week 2 Notes Winter Quarter
Intro to Psychological Science Week 2 Notes Winter Quarter PSYCH 1001 - 02
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This 8 page Class Notes was uploaded by Matthew Stein Oakley on Sunday January 31, 2016. The Class Notes belongs to PSYCH 1001 - 02 at University of Denver taught by UNI Staff in Winter 2016. Since its upload, it has received 12 views. For similar materials see Introduction to Psychology in Psychlogy at University of Denver.
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Date Created: 01/31/16
Medulla – basic bodily functions such as breathing, heart rate Left signals go to right hemisphere, right signals go to the left hemisphere NOT THE SAME FOR VISION Medulla at the intersection of both hemispheres Cerebellum – coordinated motor movement (regulates muscle activity) Reticular formation – a diffuse network of nerve pathways in the brainstem Connects spinal cord, cerebrum, and cerebellum Mediates overall level of consciousness Thalamus – controls where messages go Center for pain perception, relays sensory information Hypothalamus – coordinates both the autonomic nervous system and activity of the pituitary gland Controls body temperature, thirst, hunger (autonomic) Homeostasis Involved with sleep and (particularly) negative emotional activity Sex drive The “pleasure center” or “reward center” is the medial forebrain bundle which runs from the midbrain through the hypothalamus and nucleus acumbens. It appears that virtually all addictive drugs exert their influence by increasing dopamine levels in the reward center. Basal Ganglia – part of dopamine network, linked to thalamus and involves coordination of movement Cocaine – blocks reuptake of dopamine, norepinephrine, and serotonin Amphetamines – increase levels of dopamine, norepinephrine, and serotonin Nicotine – mimics Ach, increases dopamine It is believed that a key component of addiction is the positive emotional effects of dopamine. Hippocampus – responsible for particular memory from personal experiences EMOTION EMOTION Traditional View of Emotions: Stimulus situation Emotion Arousal (shark attack) (fear) (pounding heart) James-Lange Theory of Emotions: Stimulus situation Arousal Emotion Cannon-Bard Theory: Stimulus situation Simultaneous arousal and emotion Schachter & Singer (1962): Gave shot of epinephrine, but told Ss it was a vitamin 3 groups of subjects: o Gr 1: Told shot has no side effects o Gr 2: Told shot would lead to numbness in feet, itching, slight headache (wrong symptoms) o Gr 3: Told correct symptoms – increased heartrate, feeling flushed Told to wait in waiting room Joined by confederate who was either really pissed or very happy Two-Factor Theory of Emotions Stimulus situation Arousal Cognition Emotion: Pounding heart jogging no emotion Pounding heart racing excitement Pounding heart being chased FEAR Fast & Slow Pathways to Emotion - The thalamus sends signals to BOTH the amygdala and the cortex o The signal sent to the amygdala generates a very quick emotional reaction o The cortex analyzes the stimulus and sends its evaluation to the amygdala. If the cortex determines there is no threat, the emotion is inhibited. - Stimulus situation THALAMUS AMYGDALA Fear (emotion) - FAST THALAMUS CORTEX AMYGDALA Fear (emotion) SLOW EMOTION – A response of the whole organism involving: 1. Physiological Arousal 2. Expressive Behaviors 3. Conscious Experience -We use 100% of our brain, what isn’t firing is just as important to our understanding of something that is firing. CORTEX (4 lobes) - Frontal - Temporal - Parietal - Occipital Action potential – receives information at the dendrites, axon either fires or doesn’t fire. -transition down axon is ELECTRICAL - More positive on the outside, negative on the inside - 2 mph – 80 mph speed -Myelin sheath speeds up transmission -One of many glial cells to support neuron -Myelin develops until age 25 Each neuron has a different threshold o The stronger the stimulus, the more the neuron will fire Your brain is a binary computer Between neurons, connection becomes CHEMICAL between separate neurons LOCK & KEY SYSTEM Neurotransmitter molecule a specific key to receptor site on receiving neuron o Agonist mimics neurotransmitter (acts like neurotransmitter) o Antagonist blocks neurotransmitter (makes nothing happen) Too much neurotransmitter will be present if: Cells produce too much A drug mimics the neurotransmitter A drug prevents neurotransmitter breakdown A drug prevents the reuptake of the neurotransmitter The body is overly sensitized to the neurotransmitter Too little neurotransmitter will be present if: Production is inhibited Cells producing it are damaged or killed A drug breaks down the neurotransmitter A drug prevents the reception of the neurotransmitter Acetylcholine (Ach) – influences movement, memory, attention, dreaming, sleeping Found at the union of axons and muscles as well as in brain. Responsible for the activation of muscles Factors leading to too much o Black widow venom – stimulates Ach release o Mamba venom – Prevents Ach breakdown o Sarin (and other nerve gasses) – Prevents Ach breakdown Factors leading to too little Ach o Botulism toxin – blocks release of Ach o Curare, Cobra venom – Prevent absorption of Ach o Alzheimer’s Disease – Degeneration of brain cells that produce Ach Serotonin and Norepinephrine Norepinephrine associated with increased arousal. Serotonin associated with mechanisms of sleep and arousal. Reduced sensitivity to both associated with mood disorders. Lithium - Decreases amount of norepinephrine Beta Blockers - Block receptor site for norepinephrine Prozac (SSRI) - Interferes with reuptake of serotonin LSD - Mimics Serotonin GLUTAMATE Excitatory neurotransmitter; facilitates information transmission Related to learning and the formation of memories Too much glutamate can overstimulate brain and lead to seizures GABA (gamma-aminobutyric acid) Inhibitory neurotransmitter; reduces neural activity Related to learning and the formation of memories Used to combat seizures and is being tested as a treatment for anxiety DOPAMINE Influences movement, learning, attention, motivation, pleasure and emotional arousal Parkinson’s disease results from too little dopamine Schizophrenia related to excess dopamine Critical component of the pleasure response and addiction RESERPINE o Depletes supply of dopamine CHLORPROMAZINE o Blocks the reception of dopamine L-DOPA o Stimulates production of dopamine Dopamine – influences movement, learning, attention, motivation, pleasure and emotional arousal - Parkinson’s disease results from too little dopamine - Schizophrenia related to excess dopamine - Critical component of the pleasure response and addiction Reserpine – depletes supply of dopamine Chlorpromazine – blocks the reception of dopamine L-dopa – stimulates production of dopamine Endorphins – we produce our own indigenous morphine - Exercise Sympathetic Nervous System – fight or flight response Digestion, sweaty palms, peeing when scared Parasympathetic Nervous System – controls sexual arousal