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69 Cards in this Set

  • Front
  • Back
difference between learning and memory
learning: acquiring new info
memory: store and retrieve info
Karl Lashley
rat lesion studies to find cortical area critical for memory (using mazes)

concluded that large areas are required for memories and lot of compensation (no clear localization of memory in the brain)
Law of Mass Action
(Karl Lashley)

The severity of the memory impairment for maze performance correlated with the SIZE of the cortical area removed and not with its specific location
Patient HM
(Scolville and Milner)

Young HM had seizures
removed left and right hippocampi, but discovered he had a profound memory deficit

Major Findings:
Memory could be impaired selectively without loss of other cognitive functions
Memory function is localized to the medial temporal lobes
The hippocampus thought to be a key structure for memory, but the impairment may be due to combined damage of the hippocampus and the amygdala – localization of memory not completely clear.
Anterograde amnesia
inability to form new memories after onset of a disorder (completely impaired)
Retrograde amnesia
the loss of memories formed before onset of amnesia (partially impaired)

MTL is critical for the initial formation/encoding of new memory but not the place where well-established long-term memories are stored
What could HM learn and remember?
Motor Procedural memory: part of what is called non-declarative memory (completely spared)
LONG TERM MEMORY
- declarative: things you know that you can tell others
- non-declarative (procedural): things you know that you can show by doing
DECLARATIVE memory
Conscious

Semantic memory – Memory for facts (knowing the capital of France)
Episodic memory – autobiographical (remembering your first day in school)

MEDIAL TEMPORAL LOBE
NON-DECLARATIVE memory
Unconscious

Skill learning – learning to perform a task requiring motor coordination (Mirror drawing or mirror reading)

Priming- being more likely to use a word you heard recently

Conditioning – the association of two stimuli, or of a stimulus and a response (Pavlov’s dog experiment)
Mishkin study
Delayed non-matching-to-sample task: must choose the object that was not seen previously

Bilateral and hippocampal lesions/ Medial temporal lobe damage causes impairment on this task.
Theory of Consolidation
1) You need your MTL to make new declarative memories

2) The MTL remains important for a variable amount of time as memories “consolidate” or strengthen with practice.

3) Ultimately, the memories appear to reside in the same cortical areas that initially processed them and are no longer dependent on the MTL.
Synaptic reorganization

PLASTICITY
Structural changes at the synapse may provide long-term storage and new synapses may be formed!

similar to digit amputation of D3, thalamic input from D2 start to invade D3s space. also extensive stimulation of D2 and D3 --> inputs D1 retract, inputs of D2 invade D1s location

after training/learning: more NT release, bigger EPSP, bigger and more sensitive post synaptic membrane, entire synapse enlarges
Hebb's Law
Synapses grow stronger when the presynaptic neuron repeatedly causes the postsynaptic cell to fire

Cells that fire together, wire together
Why use aplysia?
used to study plastic synaptic changes in neural circuits because it has fewer nerve cells + create detailed circuit maps in invertebrate ganglia – little variation between individuals

has a siphon, if stimulated with touch, gill withdrawal reflex
Habituation in aplysia
After repeated squirts, the animal retracts the gills less – it has learned that the water poses no danger.

Caused by synaptic changes between the sensory cell in the siphon and the motoneuron that retracts the gill

Less transmitter released in the synapse results in less retraction.

Over several days the animal habituates faster, representing long-term habituation.

The number of synapses between the sensory cell and the motoneuron is reduced.
Long term potentiation (LTP)
What is tetanus?
a stable and enduring increase in the effectiveness of synapses

Synapses in LTP behave like Hebbian synapses:

Tetanus drives repeated firing
Postsynaptic targets fire repeatedly due to the stimulation
Synapses are stronger than before
Tetanus
a brief increase of electrical stimulation that triggers thousands of axon potentials

After tetanus, EPSPs remain high.
LTP Process
The CA1 region has both NMDA and AMPA receptors.
Glutamate first activates AMPA receptors.
NMDA receptors do not respond until enough AMPA receptors are stimulated and the neuron is partially depolarized.
NMDA receptors at rest have a magnesium ion (Mg2+) block on their calcium (Ca2+) channels.
After partial depolarization the block is removed and the NMDA receptor allows Ca2+ to enter in response to glutamate.
William James theory of emotion
emotional stimulus goes to cerebral cortex and turns into bodily response
then you recognize that and feel the emotion

we are afraid because we run.
Walter Cannon theory of emotion
disagreed with James - Many emotional situations produced the same kind of bodily emotional response
You already feel the emotion before the stress response
Emotion does not depend on the cerebral cortex because you can elicit “sham rage”

Cannon and Bard proposed circuit:
emotional stimulus
thalamus and hypothalamus
cortex
feelings
bodily response

cut out cortex and hypothalamus found that animals couldnt elicit sham rage
Papez theory of emotion
limbic lobe of the cortex

hypothalamus to
anterior thalamus
cingulate
hippocampus
Kluver Bucy theory of emotion
hyper oral, hypersexual tendencies, and psychic blindness (which is not being able to tell which objects should go in mouth) seen in animals

These Studies added the hippocampus and amygdala
to the list of “emotional” structures.
MacLean theory of emotion
added amygdala to limbic lobe in the proposed circuit

he was known as the great synthesizer
WHAT’S WRONG WITH LIMBIC SYSTEM THEORY
1) Limbic System has never been satisfactorily defined

1) System was proposed to be an emotion and not a cognition system, but later research showed that a major limbic area (hippocampus) is crucially involved in cognitive memory

3) Most limbic areas have not been implicated in emotion

4) In attempting to explain all emotions at once, it explained no emotions very well.
Downer experiment
identified amygdala as key structure in emotion

using monkey brains, amygdala lesion only on left side.
transected optic chiasm and corpus callosum.

show a picture of scary snake on left side, monkey shows no fear. show it on the right side, monkey screams
Fear conditioning
rats hear a tone, tone paired with electric shock, tone elicits fear responses

US – Unconditioned Stimulus (Shock)
UR Unconditioned Response (Freezing)
CS Conditioned Stimulus (Tone)
Classical Pavlovian conditioning
US – Unconditioned Stimulus (mint) (food)
UR- Unconditioned Response (mouth feeling dry) (salivating)
CS- Conditioned Stimulus (computer tone) (bell)
Low road to fear
sensory thalamus --> amygdala
High road to fear
sensory thalamus --> sensory cortex --> amygdala
Amygdala circuit (Joe LeDoux)

CS pathway
CS
auditory thalamus
auditory cortex
lateral amygdala
Amygdala circuit (Joe LeDoux)

US pathway
US
somatosensory thalamus
somatosensory cortex
lateral amygdala
Amygdala circuit (Joe LeDoux)

CR pathway
lateral amygdala
central nucleus
hypothalamus that mediates fear responses like freezing, higher blood pressure, stress hormone release
Bilateral Amygdala lesion
impair the use of information from the eye region

unable to differentiate emotions on the face (i.e looking randomly at the nose which doesn't give emotional info unlike eyes and mouth)
LTP in the amygdala
LeDoux and Staubli

hypothesis of having more AMPA receptors enter the brain during (fear) conditioning (which strengthens the synapse)

also played the tone not paired with the shock

conclusion: Natural learning can induce LTP in the brain!
What is the literal meaning of the word schizophrenia?
Schizein = “to split”
Phren = “mind”
Schizophrenia: abnormal genes
Neuregulin 1 (participates in NMDA, GABA and Ach receptor regulation)
Dysbindin – implicated in synaptic plasticity
COMP- involved in metabolizing dopamine
Disrupted Schizophrina 1 gene (DISC1) – abnormal in a Scottish family with a high incidence of schizophrenia

identical twins- they don't both have schizophrenia
Schizophrenia: brain structure abnormalities
enlarged ventricles
cellular disarray of the hippocampus-- hippocampus smaller
accelerated loss of gray matter in adolescents-- especially affecting temporal lobe (high level vision), primary motor and somatosensory cortices
hypofrontality hypothesis
damage to the prefrontal cortex

patients perform very similarly on a card sorting task as people with frontal lobe damage
dopamine hypothesis
Schizophrenia results from either excessive levels of synaptic DA or excessive postsynaptic sensitivity to DA

DA antagonists relive amphetamine psychosis (disorder with similar symptoms to schizophrenia)

use neuroleptic drugs!
problems with dopamine hypothesis
but for some people, neurotransmitters other than DA can be inhibited

Many schizophrenic patients have normal levels of DA metabolites
Many schizophrenics have normal densities of DA receptors
Neuroleptics work very slowly at the behavioral level but fast at the receptor level
Many patients are insensitive to neuroleptics but sensitive to atypical neuroleptics
Atypical neuroleptics increases DA in the frontal lobe?!
glutamate hypothesis
Schizophrenia may result from under-activation of Glutamate receptors
depression: genetic
There is a clear genetic component
-60% concordance with identical twins
-20% concordance with dizygotic twins
-Adoption studies consistent with genetic component
depression: brain changes
Increased blood flow in PFC and Amgydala.
Decreased blood flow in parietal and posterior temporal cortex and anterior cingulate
What does environmental enrichment do for your brain?
Increases cortical thickness
Increases number of synapses
Increases in dendritic branching
Increases number of blood vessels (more oxygen, nutrients)
increases BDNF
Increases NEUROGENESIS (The birth of new neurons) in the hippocampus (dentate gyrus) and olfactory bulb
BDNF
Brain Derived Neurotrophic Factor

In development: Helps young neurons grow.

In Adults: Is neuroprotective from ischemic damage and potentiates synaptic transmission.
Morris Water Maze
used to study hippocampal function in rodents

enhanced neurogenesis is associated with improved spatial memory performance in animals, but also, learning itself may also stimulate neurogenesis…. What comes first?
Studies in humans: correlation study
In older adults:

OUTCOME: MORE PHYSICAL ACTIVITY IS CORRELATED WITH LOWER RATES OF DEMENTIA
Studies in humans: intervention study
(Colombe)
Subjects 60-79 years old subjects, half participated in a 6 month aerobic exercise program, half did toning & stretching.
Results: Aerobic exercise participation resulted in significant increases in brain volume in the frontal lobes compared to toning & stretching group
Effects of exercise in healthy young adults
Students in the “Exercise” course got significantly faster at answering a recognition memory test compared to the control task!
effects of exercise on depression
-only long walks improve mood
-exercise is as good as antidepressant Zoloft at 4 months, and even better than it after 6 months
-medications increase BDNF, exercise increases BDNF
You shake a guy's hand and you receive a shock. You come back next week.

Hippocampal lesion?
Amygdala lesion?
Hippocampal and amygdala?
Hippocampal lesion? hesitant about shaking your hand...I don't like you, but I don't know why.
Amygdala lesion? would shake your hand again...it doesn't scare me.
Hippocampal and amygdala? as if the complete episode did not happen.
Major functions of the Frontal lobes
Social Emotion
Cognition:
-Working Memory
-Task Shifting
-Attention
working memory
delayed response task
keeping things in mind (comparing prices, remembering phone number)

delayed response task for monkeys: dorsal lateral prefrontal cortex tiny lesion, but couldn't remember where food was

occulomotor delayed response task: fixate on a point, shown a cue in space, delay, eye movements respond to cue
task shifting
wisconsin card sort task
don't know which to match (by color? by shape?), the rule can change at any point
attention
overt attention: when eye movements allow the focus of our attention to coincide with point of fixation
covert: focus of our attention is directed not on the point of fixation

posterior parietal cortex (showing spatial neglect: cannot attend to one side of the visual cortex), superior colliculus, frontal eye field (which is just in front of the motor cortex)

dysfunctions of attention -- neglect
brain areas important for improv
medial prefrontal cortex activated

dorsal lateral prefrontal cortex and lateral orbital frontal cortex are deactivated during improv, releasing from your inhibitions
Three Types of Affiliative Behaviors
Parent-Child
Filial
Male-Female/Partner
What is the hypothalamus good for?
2 Key Nuclei in the hypothalamus:
Supraoptic Nucleus
Paraventricular Nucleus

2 Key neuropepties:
Vassopressin
Oxytocin

neurosecretory cells with axons that go to posterior pituitary gland (secretes hormones)
Prairie voles vs. montane voles
prairie: monogamous, live in multigenerational family groups, both parents take care of young, territorial/reject intruders

montane: promiscuous, social isolation, little parental care
How do pair bonds form in prairie voles?
female juvenile voles come across the urine smell of an unrelated male
mate for 30-40 hrs
!!
female choice test
female goes to male partner's cage over neutral or stranger cage
Females:
if we inject oxytocin, vassopressin, oxy RA, vasso RA
Unmated females: if we inject oxytocin, time spent with stranger male increases/ if we inject vassopressin, time spent with stranger male slightly increases.

In mated females: if we inject oxytocin receptor antagonist, prevents change in behavior/ vassopressin receptor antagonist does not change her at all
oxytocin and vassopressin surge....
oxytocen surges in females after mating
vassopressin surges in males after cohabitation
Males:
if we inject oxytocin, vassopressin, oxy RA, vasso RA
Unmated males: if we inject oxytocin, time spent with stranger female slightly increases/ if we inject vassopressin, time spent with stranger female extremely increases

In mated males: if we inject oxytocin receptor antagonist, no change/ vassopressin receptor antagonist extreme decrease
Mice can be genetically engineered to be
More affiliative by inclusion of the Prairie
Vole vasopressin Gene
extreme increase in affiliative behavior
neurobiology of love in humans
Lots of overlapping activated areas between maternal and romantic love.
Activate areas involved in both reward and affiliative behavior (with high oxytocin and vasopressin receptors)
Both forms of attachment suppress activity in regions associated with negative emotions (amygdala & prefrontal regions).
Conclusion: Attachment processes may employ a push-pull mechanism that activities specific pathways of reward and affiliation and at the same time suppresses brain areas involved in negative emotions.
LTP of the hippocampus (story)
(trisynaptic circuit)
inputs from the entorhinal cortex project to dentrate gyrus (via the perforant path and mossy fibers) and then projects to CA3 (has schaffer collaterals) and then goes to CA1

can show artificial learning/ LTP in the hippocampus
what does exercise do alone?!
improves spacial memory functions