Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

59 Cards in this Set

  • Front
  • Back
Cellular Mechanisms of Learning
– The process by which experiences change our nervous system and hence our behavior
Stimulus-response learning
– Learning to automatically make a particular response in the presence of a particular stimulus
– Includes classical (Pavlovian) and instrumental (Skinnerian/Behaviorist) conditioning
Classical Conditioning
The process by which a stimulus that initially produces no particular response (the conditioned stimulus or CS) is followed several times by a stimulus (the unconditioned stimulus or US) that produces a response (the unconditioned response), which results in the conditioned stimulus leading directly to the response (a conditioned response). (Ex. Salivating; Watson and rat fear)
Cellular Mechanisms of
Classical Conditioning
Hypothetical circuit:
US (food delivery) – neuron in ss systems delivers a strong synapse and induces salivation.
CS (1000 Hz tone) – neuron in auditory system delivers a weak synapse. But repeated pairings leads the tone to induce a strong synapse and salivation on its own
Strengthening Synapses
Donald O. Hebb (Canadian Psychologist)
– In 1949 hypothesized that coordinated activity of a presynaptic terminal and a postsynaptic neuron strengthens the synaptic connections between them
– Hebbian hypothesis: “Neurons that fire together wire together”
Long-term potentiation
– A long-term increase in neuronal excitability in response to a particular input
– A long-term increase in neuronal excitability in response to a particular input
The Hippocampus
C-shaped, deep in cortex/dorsal ventral in rats, downward/ventral in humans b/c of enlarged frontal lobe.
Input through perforant path: synapses on dendrites of granule cells w/in dentate gyrus, excitatory. Granule cells send axons to (via mossy fibers versus schaffer collateals) CA3 pyramidal cells. CA1 Pyramidal cells send projections out of pyramidal; all excitatory synapses.
1) Strong depolarization pulses paired with EPSPs (when schaffer collaterals are stimulated). 3) Stimulus of same strength (weak stimulus with strong postsynaptic stimulus – strong long term increase (LTP))
Important Principles of LTP
 Specificity—only those synapses that are correlated with post-synaptic activity should be strengthened
 Associativity—those synapses that fire coincidentally with post-synaptic activation should be strengthened
stimulate both axons of CA3 pyramidal cells and record/stimulate CA 1 pyramidal cell.
Pathway 1: Increase synapse strength after Tetanus (a rapid stimulation) versus before Tetanus. Induces LTP in recording from CA1.
Pathway 2: Other synaptic pathways are Not strengthened. After tetanus to pathway (no change with titanic stimulus).
Associativity of LTP
Some energy goes passively (not via Na+ channels) up dendrites – dendritic spike (dopolarization). Action potential reaches terminal: Glu released. Increase in resting membrane potential. LTP, synapse strengthened. If dendritic spike at the same time as synapse fires: LTP.
??Weakening/elimination of synapses not associated with output.
Role of the NMDA Receptor
At resting potential: Action potential, Glu released into postsynaptic space. Mg2+ blocks NMDA receptors even though Glu binds. Only Na+ ions come in through AMPA receptors.
Depolarization: Unblocked Mg2+ from NMDA. Binding of Glu also to NMDA; Ca2+ comes through NMDA causing more AMPA receptors to appear in postsynaptic membrane. More Glu binding sites leads to more Na into postsynaptic cell. Larger postsynaptic potential (*No LTP without NMDA receptors which release Mg2+ at Ca entry). More na to postsyn.
AMPA Receptor Insertion
 Fluorescent-labeled AMPA receptors
Before stimulus spine 2 is not visible, but after stimulus it is because of fluorescent labeling. *to see if they were getting more ampa rec added with ltp (due to tet stim) by seeing brightness. Provided tet stim by pathway synapsing on spine 2 which is now much brighter than before. (2 microns)to see if they were getting more ampa rec added with ltp (due to tet stim) by seeing brightness. Provided tet stim by pathway synapsing on spine 2 which is now much brighter than before. (2 microns)
The gill-withdrawal reflex in Aplysia (LTP/Learning Mechanism)
Touch siphon, gill withdraws
24 sensory neurons, 6 motor neurons
Repeated touching of the siphon leads to decreased magnitude of withdrawal (to enable it to breathe again) – Habituation
1) Each touch fully activates sensory neurons; no deduction in number of action potentials (versus wearing a watch); a postsynaptic versus a presynaptic event. Same signal to motor neuron.
2) However, less calcium enters the terminal in response to each action potential; pools of transmitter are depleted. (Ca from extracellular space used up; fewer available)
3) ****Less transmitter is released by presynaptic terminal
4) Therefore, each touch generates fewer action potentials in motor neurons.*****
5) *****Less contraction of gill-retractor muscle.
(After a while more Ca will become available)
 Pair siphon touch with strong tail shock (similar to classical conditioning)
 Magnitude of gill withdrawal in response to siphon touch increases. (Strong stimulus can elicit hypersensitive reaction).
1. A strong shock to the tail activates the tail sensory neurons
2. Tail sensory neurons activate “facilitory” (increase firing of other cells) interneurons that synapse on terminals of siphon sensory neurons
3. “Facilitory” neurons cause more calcium to enter terminals of siphon sensory neurons. (Axoaxonic synapse)
4. More transmitter is released by presynaptic terminal
6. The strength of the gill retraction increases.
5. This generates more action potentials in motor neurons.
- Test learning by testing habituation. Ex. Infant attention signals that learning has occurred; problem with Ca depletion as habituation.
Kinds of memory
 Iconic
 Short-term
 Intermediate-term
 Long-term
 Permanent
Go back and forth from immediate to working and then consolidated into long-term. All are interrelated and can be forgotten.
Ionic vs Short-term
Photographic memory for a few seconds. Lasts for a short time. --Short term: Seconds to minutes
Intermediate versus long-term vs permanent
Int: not permanent, ex. parking car. Lasts for about a day. Long: ex. locker combination (yr?) Permanent: your name.
Categories of Memory: Declarative vs nondeclarative
Declarative: daily episodes (episodic); words and their meanings (semantic), history (during lifetime events; names; events of others).
Motor skills/procedural; Associations; Priming cues (ex. the hook of an umbrella); Puzzle solving skills. Cannot describe; not consc. aware of. May cue an assocation with an object.
Brain areas involved in declarative memory disorders
(Hippocampus is involved in storage of some memories and forming new memories)
Prefrontal cortex. Basal forebrain. Fornix. Thalamus (big oval below fornix). Mammillary body (small circle below thalamus). Amygdala (almond below mam. body). Rhinal cortex (furthest distal). Hippocampus: right side and below thalamus.
.M. (Henry M.) suffered severe epileptic siezures since he was about 10 years old
Referred in 1953 (age 27) to William Scoville
Bilateral removal of the hippocampus and perihippocampal temporal lobe structures.
H.M. and memory loss
.M. was examined in 1955, 19 months following the surgery
Gave the date as “March, 1953”
Gave his age as 27
Could not remember talking to anyone before he entered the examination room
Denied having had surgery.
H.M. learns new tasks/skills:
[Could use nondec mem as for drawing b/c hippocampus not needed. Helps however for *spatial memories.]
as well as any non-amnestic person. Procedural memory works (think he's never done task before) (sep part of brain). No longterm memory.
Spatial learning and memory in rats
Morris Water Maze. Hippocampus lesioning made it just as difficult to find platform as in first trial.
Acquisition and storage of declarative information:
[Possible declarative memory storage sites diag: covers three corners of brain]
Longterm storage: a variety of cortical sites: wernicke's area of the meanings of words, temporal cortex for the memories of objects/faces, etc.
Shorterm: Hippocampus and related structures.
Acquisition and storage of nondeclarative information:
Long: Cerebellum, basal ganglia, premotor cortex, and other sites related to motor beh. [CBC or CerBasPremo]Short: sites unknown but presumabely widespread.
Disorders of Memory
[Korsakoff’s Syndrome: severe anterograde amnesia, usu due to chronic alcoholism; caused by damage to temporal lobes; HM; failure of relational learning]
Anterograde vs. Retrograde Amnesia
Hippocampus and Medial Temporal Lobe
Vitamin B1 Deficiency
Korsakoff’s Syndrome
Medial Thalamus and Mammillary Bodies
Alzheimer’s Disease
Neurofibrillary Tangles (yellow triangles) and Amyloid Plaques
(big brown)
Emotions: Theory
James/Lange Theory of Emotion (mid-1880s)
Emotions arise from physiology and experience (Sep events)
Activation of sympathetic NS prepares an organism for action (behavioral activation)
Activation of parasympathetic NS allows for energy storage (behavioral suppression)
Emotions, therefore, are coactivated with peripheral neural activation
Evidence: Muscle-by-muscle instructions for simulating emotional faces results in measurable autonomic changes (heart rate, skin conductance)
Thus, one source for emotion is the sensory drive from muscles and viscera
Emotions: Two-Factor Theory
Stanley Schachter & Jerome Singer (1962)
Emotion depends on 2 factors:
Physiological arousal
Cognitive interpretation of arousal
Unless you can interpret, explain, and label the bodily changes, you will not feel a true emotion.
- Mid 1900s, fMRI: brain struc and emotion...
William James
I say that for us emotion dissociated from all bodily feeling is inconceivable. (1893)
Need physiol component.
Sham Rage
Phillip Bard (1928) showed that bilateral removal of cortex resulted in aggressive
behavior with no obvious target (“Sham rage”)
Bard concluded that while the cortex was important for the subjective experience
of emotion, the expression of emotional behaviors did not require the cortex.
Walter Hess later showed that electrical stimulation of the hypothalamus could elicit
rage and attack behavior. Cut cerebral cortex off from pons, (Midbrain) and medulla.
Hypothalamus and Aggression
(Cortex was not nec For raage but for to inhibit.
Jose Delgado’s Bull: inhibited hyp to stop charging. Eggar and Flynn’s Cats: medial hyp: aggression. Lat hyp: aggression focused to attack prey; quiet biting attack.
Role of Orbitofrontal Cortex
Phineas Gage
Foreman on railway construction
Using a steel rod to blasting powder into a charge hole
OOPS! The charge went off…(just one example of why women live longer than men)
Remarkably, Gage survived
What happened?
Gage lost control of his personality
Seemed to lose “executive functions”
Unable to make or carry out plans
Displayed inappropriate social behavior
Lost his character; “Gage was no longer Gage”
Role of prefrontal cortex is linked to planning and control of aggression
Emotional expression is distinct
(Volitional and emotional)
Voltional mov: descending pyramidal and extrapy projections from motor cortex and brainstem. Divided into Lateral (fine control of distal extremities) and medial (posture, proximal extremities).
Emotional expression:
Descending extrapy projections from limbic centers of ventralmedial forebrain and hypothalamus. Medial (gain setting, rhythmical reflexes) and Lateral (specific emotional behaviors)
First to brainstem reticular formation or straight to motor neuron pools:
Volitional mov side: motor neurons of cranial nerve nuclei and ventral horn -- Muscle contraction and movement. (motor, voluntary)
motor neuron pools: (Side of emotional expression)
Autonomic preganglionic neurons -- Activation of smooth muscle and glands. (invol: smooth musc)
Voluntary Paresis
[Inability to express appropriate emotion]
Facial motor paresis is an inability to form the voluntary smile but the response to humor smile is intact. (Pyramidal lesion)
Emotional Paresis
[Either may result from traumatic injury]
Voluntary smile is in tact but not response to humor. Duchenne.
The “limbic lobe"
Past: mainly cingulate gyrus and parahippocampal gyrus.
Involves many structures. Corpus callosum and further to the front. ***Orbital and medial prefrontal cortex. Cingulate gyrus; parahippocampal gyrus. See diagram: ventral basal ganglia; anterior commissure; mammillothalamic tract; anterior nuc of thalamus; fornix; mediodorsal nuc of thal...
Klüver-Bucy Syndrome
Bilateral removal of temporal lobes in rhesus monkeys led to:
Visual Agnosia
Strange oral behaviors
Lack of fear, excitement, anger and related vocalizations
Later found that these behaviors could be elicited by selective removal of the amygdala
John Downer (1950s)
Unilateral removal of Amygdala and commissural structures
Produced a “Unilateral Klüver-Bucy Syndrome”
(Same half vs presented to other side leads to a lack...)
The Anatomy of the Amygdala
See diag. Amydala: central group on top, medial group on outer sides, basal lateral group in middle.
Fear and the Human Amygdala
Rare disorder (patient SM): selective deterioration (only for amygdala; bilaterally) Hippocampus is intact. No fear response (cannot recog nor express).
The Anatomy of the Amygdala
Orital and medial prefrontal cortex leads to Amygdala (basal-lateral nuclei) and to Mediodorsal nucleus of thalamus. Amyg leads to (Orbital and medial) and ventral basal ganglia which leads to Mediodorsal (which leads to Orbital and medial)
1) Primary reinforcers (taste, touch pain); 2) Neutral sensory stimuli (visual, auditory stimuli related to an object) Learnign area of neuron.
Orbital and medial prefrontal cortex: implicit motor actions. Explicit conscious processing to obtain rewards, avoid punishers, and implement longterm plan. Hypothal and brainstem: visceral motor effector system to prepare body for action.
Model for the awareness of emotional feelings
Triggering stimuli lead to either Amygdala-dependent associative learning or Hippocampal-dep explicit memory which also interact with each other. Stimuli may also lead straight to Immediate conscious experience of emotional feelings. Amyg and hipp-dep also lead to immediate conscious exp of emotional feelings.
1) The amygdala:
2) Inc activity of serotonergic synapses:
1) contains many benzodiazepine rec. Lesions impair recog of fear, Not produc of facial exp of emotion (vs basal ganglia and disgust) 2) Inhibits aggression. Low serotonin: increased risktaking. (Opp of stimulate hippocampus-aggression)
Hebb Rule:
--The size of the first popul epsp indicates the strength of the:
A synapse will be strengthened if it repeatedly becomes active around the same time the postsyn neuron fires. --synaptic connections before longterm potentiation takes place.
Nitric oxide:
--Damage to the inferior temporal cortex disrupts the ability to:
May be produced in the dendritic spines of the hippocampal formation. --Recog familiar objects.
--Implied mov photographs activate:
--Ventral stream ends in the:
--Area MT/MST --Temporal lobe; Where. (VTE vs DPA)
Synaptic changes responsible for acquiring a classically conditioned emotional response occur in the:
--In humans the basal ganglia: - Stimulate this area of brain for animal training:
Lateral amygdala. - plays an important role in automatic, nondeliberate learning. - Medial Forebrain bundle (MFB)
The three inputs to the VTA that play the most important role in reinforcement:
--Anterograde amnesia
Amygdala, lateral hypothal, prefrontal cortex. VTA has reinforcing effects as for addictive drugs --Loss of relational learning.
Neurons in field CA1 of the hippocampus are easily damaged when metabolic disturbances set off a series of events that include the: --Task for navigation activates:
Entry of ca into the neurons. --Left hippocampal formation.
Ventromedial prefrontal cortex
Includes the orbitofrontal cortex; important role in emotional reac. Communic w/ temporal pole, amygdala, other limbic parts. Damage: problems describing situations occuring to them. Prefrontal cortex for moral judgments. (Low level of activity in criminals and low gray matter; 5HT input)