Download Final Exam Study Guide (rtf)

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Holonomic brain theory wikipedia , lookup

Neural correlates of consciousness wikipedia , lookup

Transcript
Final Study Guide
COGS 107C
Spring 2008
I. 13 Brain Facts
Know examples of the following subset of brain facts:
a. Specialization of function
b. Classical & nonclassical receptive fields
c. Parallel architecture
Know the following subset of brain facts:
a. There are about 1012 neurons and 1015 synapses in the human brain
b. Each neuron is connected to approximately 3% of neurons in the surrounding
mm2
c. The effect of one cell on another is about 1-5% of firing threshold
d. An action potential lasts about 1 msec
e. Synaptic transmission takes about 5 msec
f. Synaptic potentials can last from 1 msec to many minutes
II. Common Methods in Cognitive Neuroscience
Be familiar with the following methods for measuring and/or manipulation the structure
or function of the nervous system:
a. fMRI
b. EEG/MEG (ERP/ERF, time frequency analysis)
c. Optical imaging
d. MRI
e. Diffusion tensor imaging (DTI)
f. Lesions
g. Transcranial magnetic stimulation
h. Microstimulation
i. Skin conductance response (SCR)
j. Temporary inactivation (e.g., via muscimol or cooling)
Specifically, for each of these you should know:
a. What each method directly measures/disrupts/drives
b. What aspect of neural activity (e.g., synaptic potentials or action potentials) each
method directly or indirectly reflects
c. The approximate temporal and spatial resolution of the method
d. Possible ambiguities of each method
e. The kinds of questions each method might be useful for addressing
You should be able to apply the six hallmarks of good results to hypothetical experiments.
Specifically, given a hypothetical experiment, you should be able to tell us:
a. What (if anything) makes these results compelling?
b. Are there any possible ambiguities/confounds in the results?
c. What might be a good experiment to follow up on this research?
III. Spatial Cognition
For the following parts of the brain, indicate:
a) How it is it involved in spatial cognition (e.g., important for
guiding/compensating for eye movement)
b) What coordinate system(s) does it use (if known)?
c) What type of stimuli/behaviors activate these cells?
Area LIP
Area VIP
Hippocampus
IV. Object Recognition
How do the characteristics of cortical areas (e.g., receptive field properties) change as
you go up the cortical hierarchy?
V. Prefrontal Cortex & Executive Function
Know the following theories of PFC function and what they do/don’t explain about PFC
function/deficits
a. Somatic marker hypothesis
b. Working memory
c. Multiple processing levels
d. Rule representation
e. Flexible, limited capacity controlled processing
VI. Classical Conditioning
You should be able to identify the following components of a given classical
conditioning paradigm:
Unconditioned stimulus (US):
Conditioned stimulus (CS):
Unconditioned response (UR):
Conditioned response (CR):
You should be able to define the following classical conditioning phenomena:
Extinction
Blocking
Overshadowing
VII. Classical Fear Conditioning
What are the CR and UR in classical fear conditioning?
What are the roles of the lateral nucleus of the amygdala and the central nucleus of the
amygdala in classical fear conditioning?
What are the routes via which the CS and US can influence the amygdala?
According to Medina et al., how does the initial neural basis of the CS-CR association
change with further learning?
What is the synaptic change responsible for learning the CS-CR association?
What is the behavioral evidence that extinction involves learning to suppress fear
conditioning, rather than unlearning fear conditioning (i.e., returning the brain to the state
it was in before it was conditioned)?
What are the roles of medial prefrontal cortex and the hippocampus in extinction of
classical fear conditioning?
VIII. Classical Eyeblink Conditioning
What are the CR and UR in classical eyeblink conditioning?
What are the roles of the mossy fibers, climbing fibers of the inferior olivary nucleus,
cerebellar cortex, interpositus nuclei, and red nucleus in classical eyeblink conditioning?
According to Medina et al., how does the initial neural basis of the CS-CR association
change with further learning?
What is the synaptic change responsible for learning in the interpositus nuclei and
cerebellar cortex?
What is the evidence (both behavioral and neural) that extinction of eyeblink
conditioning involves learning to suppress eyeblink conditioning not simply unlearning
the conditioning?
IX. Reward & Reinforcement Learning
What is the role of the following brain areas in detecting rewards, learning to predict
rewards, and/or using predicted rewards to guide behavior?
Lateral hypothalamus
Orbital frontal cortex
Ventral tegmental area dopamine (DA) neurons:
Striatum
Supplementary motor area
Dorsolateral prefrontal cortex
What are the three components of the striatum?
What is “temporal-difference learning” and what aspect of this algorithm appears to be
implemented by midbrain DA neurons?
X. Drug Addiction
What neuromodulatory system does cocaine directly act on?
What neuromodulatory system does heroin directly act on?
What is positive reinforcement?
What is negative reinforcement?
What is Solomon’s opponent process theory of motivation (A & B Process) and how does
it relate to drug use/addiction?
What is intracranial self-stimulation (ICSS)? How does ICSS change when the animal is
high or in withdrawal?
You should know that two key neuroanatomical structures involved in the “reward
circuit” activated by drugs of abuse are the nucleus accumbens and the central nucleus of
the amygdala. You should know that two key neuromodulators involved in this reward
circuit are dopamine (DA) and opioid peptides.
You should know that a key neuromodulator involved in the “anti-reward circuit”
activated by drugs of abuse is corticotropin releasing factor (CRF). You should know
what effects CRF has when naturally triggered by alarming situations and what effect
CRF antagonist has on the self-administration of alcohol in addicted and non-addicted
rodents.
What is the role of medial prefrontal cortex in addiction?
What happens to DA levels in the minutes/hours that follow using addictive drugs?
What happens to the DA system after prolonged used of addictive drugs?
XI. Music & Language
What are some similarities between language and music?
What are some key differences between language and music?
What is the Frequency Following Response and what part of the brain produces it?
How does musical training appear to influence speech perception (both behaviorally and
neurally)?
What are the musical and linguistic deficits that characterize musical tone deafness
(mTD)?
What does Ani Patel think is the neural basis of mTD?
What does Ani Patel mean when he says that mTD may be an example of a behavioral
dissociation without a neural dissociation?
What is Patel’s “shared syntactic integration resource hypothesis” and what evidence
(both behavioral and neural) is there that supports it?
XII. Language: Basics
What are some differences between language and the communication systems of other
animals?
What are Chomsky's and Elman's views on why only humans are fully capable of human
language?
What are some neuroanatomical differences between human and non-human primate
brains that might contribute to our unique capacity for language?
What evidence is there that people tend to rely more on the left hemisphere than the right
hemisphere for language?
XIII. Language: Production vs. Comprehension
What are Broca's and Wernicke's areas and what are the symptoms of Broca's and
Wernicke's aphasia?
What are the five areas Dronkers et al. found to be critical to language comprehension?
What deficits are produced by lesions of just Broca's area (or a subset of Broca's area)?
XIV. Language: Syntax vs. Semantics
What is an example of hierarchical grammatical relationships in language?
What is an example of "long distance" grammatical relationships in language?
What is an example of a recursive grammatical rule in language?
Why are many language researchers interested in contrasting the processing of syntactic
and semantic information?
What are the features of the N400 ERP component (i.e., scalp distribution, latency,
polarity)?
What type of stimuli elicit an N400 and what stimulus features affect N400 amplitude?
What cognitive functions are thought to be indexed by the N400?
If the scalp topographies of two ERP components differ, what can you infer about the
neural generators of those two ERP components?
What are the features of the P600 ERP component (i.e., scalp distribution, latency,
polarity)?
What type of stimuli elicit a P600 and what stimulus features affect P600 amplitude?
What cognitive functions are thought to be indexed by the P600?
What evidence is there that neither the N400 nor the P600 are generated by cognitive
processes specific to language?
What evidence is there that the N400 is not only an index of semantic processing?
What evidence is there that the P600 is not only an index of grammatical processing?
Contrast Hagoort's and Kuperberg et al.'s interpretation of neuroimaging investigations of
the processing of syntactic and semantic anomalies.
XV. Language: Learning
What is the "poverty of stimulus" argument for the existence of innate grammatical
knowledge like the "faculty of language narrow" (FLN) proposed by Hauser, Chomsky,
& Fitch?
How did Rodriguez et al.'s neural network learn the phrase structure grammar anbn?
What does Karl Friston think is the function of cortical feedforward and feedback
connections in perception and perceptual learning?
What are the three different theories of the neural origins of the mismatch negativity
(MMN) ERP component covered in lecture? What evidence supports Friston's
interpretation?
XVI. Social Cognition
What are observational fear learning and instructed fear learning?
What are key similarities and differences between observational fear learning and
classical fear conditioning?
What are key similarities and differences between instructed fear learning and classical
fear conditioning?
What are the neural circuits for observational and instructed fear learning proposed by
Olsson & Phelps?
What are the effects (or lack thereof) of oxytocin on social behavior (especially in the
investing and lottery games investigated by Baumgartner and colleagues)?
What is the role of the amygdala in trust and social fear and how does it appear to be
modulated by oxytocin?
What appears to be the role of the striatum in economic games and how is it or its subparts modulated by oxytocin in social economic games?