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84 Cards in this Set
- Front
- Back
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What is Learning?
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a lasting change in an organism's behavior that results from experience
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Learning can be Conscious or Unconscious
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Conscious: Memorizing a Script
Unconscious: Habituation |
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Criteria of Learning
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1.Behavior modification depends on a form of neural plasticity
2.Modification depends on organisms's experimental history 3.Modification outlasts environmental contigencies used to induce it and experience has a lasting effect on performance |
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Three ways neurons can change
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Development
Injury/Insult Experience |
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Examples of Changes in Neural Systems that have nothing to do with learning
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Instincts: Dog becomes territorial when prgnant
Innate Phobia: Monkeys and Snakes |
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Renee Descartes
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Cartesian Dualism: voluntary movement (free will) vs involuntary movement (reflexive)
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Nativism
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people have some innate knowledge
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Structuralists
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Edward Titchner
used case-studies and introspection to determine how concepts are determined from primitive sensations |
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Watson and Behaviorism
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Suggested that we need to limit our attention to events publicly verifiable
Researchers attempted to elucidate general learning mechanisms by looking at the ways subjects reacted to stimuli |
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Ethological Perspective
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recognized that learning process differed across situations and species
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Cognitive Psychology
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realized could further understand the process linking stimulus and response using scientifically defensible methods
Popular in the 1960s |
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Neuroscience
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focused on the biological mechanisms underlying learning
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Single Stimulus Learning (Stimulus Pre-Exposure Learning)
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Simplest example of learning,
How does a subject's response change when repeatedly exposed to a stimulus? |
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Possible Responses to Repeated Stimulus
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1. No effect
2. Habituation 3. Sensitization |
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Habituation
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Repeated exposure to a stimulus reduces the behavioral response
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Sensitization
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Repeated exposure to a stimulus amplifies the behavioral response
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Dishabituation
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momentary startle when stimulus changes or new stimulus occurs
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Spontaneous Recovery
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showing close to the same behavioral response prior to habituation after 24hrs rest
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Alternative explanations for reduced response
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Fatigue
Injury |
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Stimulus Generalization
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our brain assumes that stimuli that have similar characteristics will have similar consequences
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Generalization Gradient
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variation in generalization as a function of stimulus similarity
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Behaviroalists on Stimulus Pre-Exposure
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Reflexology
Lattice Heirarchy Hedonism Oponent Process Thoery of Acquired Motivation |
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Crossed Extension
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induction of one process induces a concurrent compensatory response that helps the organism adapt
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Reciprocal Inhibition
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prevents concurrent execution of stimulus-response reflexes
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Wikens
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had subjects hands strapped to a board when middle finger hit a button, then flipped the hands over and the subjects still moved finger away even though reflex was different to do so
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Hedonism
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Pleasure is the chief goal.
Behaviors that bring pleasure are strenghtend those that brings pain will diminish |
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Solomon
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Developed Oponent Process Theory
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Oponent Process Theory of Acquired Motivation
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Standard Pattern of Affective Dynamics
A process dominant when stimulus on B process slave to A process A-B equals steady state Only intensity of B process changes with experience |
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Standard Pattern of Affective Dynamics
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Stimulus on, A process kick in and peaks (affective reaction), adaption phase, steady level, B process, B peak (after-reaction), decay of after-reation
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Overmeir, Maier, Seligman
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Discovered Learned Helplessness
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Hpyoalgesia
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decreases sensitivity to pain
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Aplysia
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invertebrate sea slug;
About as big as a rat study them b/cthey are invertabrates and they have fewer bigger neurons -20,000 about 1 mm |
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Habituating Aplysia
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toughing the mantle or siphon repeated times
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Sensitizing Aplysia
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shocking aplysia before touching aplysia repeatedly
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How do neurons transport information?
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Action Potential (Mexican Waves)
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Neuron charge a rest
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-70mv
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AP Neural Charge (depolarized neuron)
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30-40mv
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What causes neurotransmitter release?
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Opening of calcium channels and folw of calcium to presynaptic membrane
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What opens calcium channels?
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The depolarization of the neuron activating the axon terminal
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What opens sodium channels?
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Activation of the Dendrites on the neuron
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How long are the sodium channels open?
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0.5-1.0 millisecs
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What does the sodium/potassium pump do?
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regulates flow of potassium and sodium in and out of the cell, ends the AP
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Basic Neuronal Pathway Underlying Habituation
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Touch (Stimulus) -> Sensory Neuron -> Motor Neuron -> Muscle (Response)
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Forces that regulate intercellular and extracellular fluids
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Diffusion and electrostatic attractions (forces)
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Diffusion
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Concentration gradient, HIGH concentration to LOW concentration
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Electrostatic Forces
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Negative ions attracted to Positive and vice versa
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Neurotransmitter Sensory Neuron Releases
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Glutimate
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How do the number of quanta released from the presynaptic neuron effect the postsynaptic neuron?
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More quanta = stronger response
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What influences how much neurotransmitter is released?
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The amount of calcium that travels to presynaptic membrane
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Basic Neuronal Pathway Underlying Sensitization
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Touch/Shock -> Sensory Neuron and facilitatory interneuron -> 2nd sensory neuron -> Motor neuron -> Muscle
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What goes on the the neuron during sensitization?
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Shocking tail increases release of 5-HT by the facilitating interneuron
5-HT binds to receptor on sensory neuron This activates G-protein G-protein activates adenylyl cyclase Adenylyl cyclase activates cyclic AMP (cAMP) cAMP activates protein kinase (PKA) PKA closes potassium (K+) channels, prolonging the action potential Prolonging action potential increases Ca2+ influx This increases neurotransmitter release onto motor neuron |
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What neurotransmitter does the facilatory neuron release?
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Seratonin (5HT)
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What are the 2 S-R pathways invovled in habituation n aplysia?
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Touching the siphon or the mantle and measuring the gill withdrawal
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Long-Term Sensitization
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Repeated shock to the tail induces gene activation
These genes code for proteins that remove part of the regulatory subunit on protein kinase Removing regulatory subunit makes protein kinase hyperactive, so it can close K+ channels for a long time This produces a long term sensitization that lasts for over 48 hours |
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Key Neuronal Change Underlying Habituation
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The Ca+ channels don't open or greatly decrease which in turn decreases the response produced by the post synaptic neuron
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Key Neuronal Change underlying Sensitization
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PKA + MaP = Creb which creates Ubiquitin Hyrolase, this allows for PKA regulartory subunit to be eaten cause [K+ channels to be closed] for a long time
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What did Hebb say about how the brain makes associations (memories)?
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Cells that fire together will wire together (1949)
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LTP Background
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Discovered by Bliss and Lomo in 1970s by their slices of the hippocamus
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Hippocamus
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part of the brain involved in forming explicit memories
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Amygdala
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part of the brain involved in making emotional memories
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Bliss and Lomo's experiment
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Hippocamus slice:
stimulate presynaptic neuron then measure data from mossy fibers postsynaptic neuron |
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LTP
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Long Term Potentiaton; post synaptic neuron has an enhanced or “potentiated” response to mild input from the presynaptic neuron
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Properties of LTP make it viable for Memory
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1) Can be unduced by brief stimuli
2) Exhibits input specificity 3) Exhibits cooperativity 4) Exhibits associability |
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3 Receptor Types Glutimate Binds to
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1. Metabotropic Receptor
2. NMDA Receptor 3. AMPA Receptor |
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When Glutimate binds to AMPA Receptor....
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A strong depolarization causes the magnesium (Mg2+) block to be removed from NMDA receptor
Now if Glutamate binds to NMDA receptor, Na+ and Ca2+ rush into cell through NMDA receptor; Na+ helps kick off new action potentials Ca2+ activates “Ca2+ calmodulin protein kinase” Ca2+ calmodulin protein kinase causes the cell to make new functional AMPA receptors New AMPA receptors make the post-synaptic cells hyperexcitable so now a little glutamate has a big impact on the post-synaptic cell |
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If Glutimate binds to NMDA receptor...
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Nothing until it binds to AMPA and gets rid of the Mg2+ plug on the NMDA channels
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What happens before LTP Mechanism...
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Strong activation of the presynaptic cell causes more releases of glutamate
This causes more Na+ to rush in through AMPA receptor on the postsynaptic cell. This depolarizes the cell (makes the inside more positive) A strong depolarization causes the magnesium (Mg2+) block to be removed from NMDA receptor |
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Nociception
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term used to refer to the perception of pain
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What neurons are sensitized during central sensitization?
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Neurons in the Spinal Cord and Aplysia
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4 Regions of the Spinal Cord
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Cervical, Thoracic, Lumbar, and Sacral
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What makes white matter different that gray matter?
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White matter transports information form one area of the body to another
Neurons in White matter are mylenatinated unlike gray matter |
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Where is the dorsal region of the spinal cord?
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The dorsal region is the region facing the back of an organism
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Noxious Stimuli
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like electrical stimulation can be used to sensitize neurons
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when was the cognitive learning approach big?
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1960s
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How long does LTP last when it is induced in anesthetized subjects?
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30min-10hrs
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How long does LTP last when induced in awake subjects?
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up to 2 weeks
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How does LTP maintain a long term effect? What signaling pathway is involved?
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Prolonging the Action Potential
PKA + MAPkinase = CREB which forms Ubiquitin Hydrolase that eats the regulatory subunit this in turn keeps K+ from reentering the cell |
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Afferent Neural Pathways
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a as in arrive
carry commands to the muscle from a processing center |
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Paw Withdrawal and Sensitization
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Before sensitization 4 secs
After sensitization 2 secs |
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Hyperalgesia
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enhanced pain reactivity
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What are the neural changes that underlie central sensitization?
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*Basically same as LTP*
Strong activation of the presynaptic cell causes more release of glutamate This causes more Na+ to rush in through AMPA receptors on the postsynaptic cell. This depolarizes the cell (makes the inside more positive) A strong depolarization causes the magnesium (Mg2+) block to be removed from NMDA receptor Now if glutamate binds to NMDA receptor, Na+ and Ca2+ rush into cell through NMDA receptor; Na+ helps kick off new action potentials Ca2+ activates Ca2+ calmodulin dependent protein kinase (CaMK II) CAMK II causes the cell to make new functional AMPA receptors New functional AMPA receptors make the postsynaptic cells hyperexcitable so now a little glutamate has a big impact on the post-synaptic cell |
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Allodynia
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a previously nonpainful stimulus (such as touch) becomes painful (Ex: sunburn)
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What neural changes lead to allodynia?
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Newmann & Woolf showed that it may be due, in part, to a phenotypic switch
Genotype of nerve cells determined by the genes found in the nucleus Phenotype of the cell is determined by the subset of genes expressed Expression of these genes is regulated by genetic, developmental, and environmental factors Phenotypic switch-a modification that alters the functional properties of the nerve cell In allodynia, A-beta fibers begin to express substance P and engage pain fibers within the spinal cord |
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DNIC
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Diffuse Noxious Inhibitory Control:
fibers that descend from the brain counter the sensitization of pain |
