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BIO SCI N113L Final Exam Learning Objectives (Lab 8: Brain-behavior…
BIO SCI N113L Final Exam Learning Objectives
Lab 3 & 4: Neurophysiology in cockroach
Measuring electrical activity
Extracellular
Measures voltage change outside of the cell
Intracellular
Measures the voltage difference between the inside and outside of the cell
Patch clamp
Measures electrical currents through single ion channels
Optical imaging
Direct visualization of voltage difference across membrane
Distinguishing spontaneous from evoked activity
Spontaneous
Neuronal firing without external stimulation
Evoked
Activity evoked by external stimulation
Identifying sensory adaptation in recorded electrical activity trace
Stimulus-duration curve
Chronaxie time
Stimulus duration required to elicit a response from the nerve when stimulating at 2X the Rheobase voltage
Larger diameter axons have smaller Chronaxie times, making them more excitable
Rheobase voltage
Weakest stimulus that will elicit any response from nerve
Factors that contribute to neuron excitability
Axon diameter
Larger diameter axons conduct signals taster than smaller axon diameters
Larger diameters reduce internal/axoplasmic resistance
Myelination
Myelin increases membrane resistance: increases axon insulation, reduces leakage of signal out of cell
Myelin reduces membrane capacitance: the amount of time it takes for the charge to build up in myelinated regions
AP needs to be rejuvenated only at the Nodes of Ranvier where there is no myelination
Single AP vs. compound AP
Compound AP (CAP)
Sum of multiple single APs firing simultaneously in a nerve bundle
Relative refractory period
Second AP has lower amplitude with same amount of stimulation, some of the axon fibers in the nerve have recovered
Absolute refractory period
Period of time when all axons within a nerve are in their absolute refractory period
Single AP
Inhibitory hyperpolarization, 2. Sub-threshold depolarization, 3. Threshold depolarization, 4. Action potential (rising, recovery), 5. After-hyperpolarization
Absolute refractory period
No amount of stimulation can trigger another AP
Relative refractory period
Stronger stimulation needed to generate another AP
Stimulus artifact
The electrical current from the stimulating pulse that is conductively passive and picked up as a signal
Saltatory conduction
Active conduction
Active maintenance of the membrane potential as it travels through the cell
Voltage-gated Na+ channels open as membrane potential reaches threshold, rejuvenates membrane depolarization before it decays
Passive conduction
Electrotonic conductance: the passive spread of membrane potentials through the cell
Involvement of channels
Voltage-gated Na+ and K+ channels clustered at nodes of Ranvier, where the AP is rejuvenated
Lab 5: Scientific communication
Independent variables
Measured by the experimenter, changes with the independent variable
Dependent variables
Manipulated by the experimenter
Controls
Negative
Group should not show the expected phenomenon, not expected to exhibit it
A baseline to compare results of experimental group(s) to
Positive
Group should show the expected phenomenon, already known to exhibit it
Validate methodology
Hypothesis
Components of a hypothesis
Testing component
Statement of the manipulated variables in the experiment
Expected result
Predicted outcome that would be expected given the proposed relationship
Proposed relationship between variables
A "mini hypothesis" guessing as to how two things are related
Vazdarjanova & McGaugh, 1999
Major findings
Rats treated with post-training lidocaine injections into the BLC had impaired memory for classical fear conditioning compared to controls
Rats treated with post-training oxotremorine injections into the BLC had enhanced memory for the context-footshock association compared to controls
Conclusions
Post-training treatments affecting BLC function modulate memory for Pavlovian contextual fear conditioning in a manner similar to that found with other types of training
Lab 6: Habituation in
C. elegans
Components of associative learning
Conditioned stimulus (CS)
A previously neutral stimulus that eventually triggers a CR after being paired/associated with a US
Unconditioned stimulus (US)
A stimulus that drives a response without training
Conditioned response (CR)
Response that is elicited by the CR
Unconditioned response (UR)
Behavior that occurs in response to the US
Association
Linkage between S-S or S-R
Experimental design
Associative vs. non-associative learning
Associative
Extinction
Pairing the CS without the US, responding diminishes over trials
Steps:
Subject detects stimulus, 2. Links perception of stimulus with response, 3. Performs the response as a result of being presented the stimulus
Non-associative
Habituation
Repeatedly presenting a novel stimulus without a US, subject stops responding to stimulus
Sensitization
Presentation of a strong stimulus enhances responses to future presentations of many different stimuli
Dishabituation
Presentation of a strong stimulus returns responding to pre-habituation levels
Minimizing variability and bias
Clearly defined set of criteria for scoring behavior
Blind experimenters, other components of experiment
Multiple data points
Calculations for tap-withdrawal trial analysis
Savings
t-test: Training trials 1-5 vs. training trials 31-35
Enhanced rate of learning during subsequent training
Learning
t-test: Training trials 1-5 vs. training trials 56-60
Dishabituation
t-test: Test trials 6-10 vs. dishabituation trials 1-5
Website for
C. elegans
genes of interest
WormBase: database that contains the entire sequence for
C. elegans
and the locations of its predicted genes
Lab 8: Brain-behavior connection and experimental design
Mass action & equipotentiality
Mass action
Cognitive functions result from coordinated activity of brain as a whole
Equipotentiality
Incomplete lesions produce deficits that can be ameliorated by time or retraining
Views of brain function
Localized view
Functions are localized to specific brain areas
Holistic view
Cognitive faculties result from coordinated activity of the brain as a whole
Patient H.M.
Experienced profound anterograde memory loss as a result of lesioning to his hippocampus and the surrounding cortex
Memory loss was only restricted to explicit memories, not implicit memories (e.g., motor skills)
Did not have as much retrograde amnesia
Conclusion from H.M.: hippocampus and medial temporal lobes are necessary for the acquisition of new memories, but are not necessary for the long-term storage of them
Tan-tan
Lesion in ventral region of frontal lobe
Allowed Bouillard to establish a connection between frontal lobes and speech
Sprague Effect
Definition
Deficits by a primary lesion can be ameliorated by a second lesion
Deficits produced by lesions are not always due to destruction of a particular region, but by the disruption of normal interaction between regions
Hemianopia
Blindness in half of the visual field produced by large lesions in visual cortex
Lesions
Types
Spare fibers of passage
Pharmacological agents
Do not spare fibers of passage
Large electrical current or excision of mass of neural tissue
These lesions confound any effects that arise from lesions since effects could be due to differentiation (destruction of afferent inputs to a particular brain region)
Limitations
Permanent damage to brain structure
Observing a deficit is not enough to conclude that the function was localized to that lesioned structure
Task performance vs. memory
Tone-shock associative fear conditioning
Dorsal PAG
Required to perform the UR, CR
Necessary for expression of all fear conditioning
Will response electrophysiologically whenever the animal is freezing
Amygdala
Required to associate the CS with the US, form a CS-CR connection
Necessary for acquisition and expression of all fear conditioning
Will respond electrophysiologically after the animal has been conditioned
Cochlear nucleus
Required to perceive the CS
Necessary for acquisition and expression of auditory fear conditioning (not contextual fear conditioning)
Will respond electrophysiologically whenever the tone is played
Extinction rates
Training context
Extinction takes longer because the subject learns to fear the context of training as well as the CS
New context
Extinction happens quicker because the subject was not trained in that context
Differences in responding in training & new context when not given CS during testing
Subject is fearful of same context in which it was trained
Lab 7: Neuropharmacology in earthworm enteric system
Neurotransmission
Steps:
Synthesis and storage
Neurotransmitters synthesized in pre-synaptic terminal or soma, store in synaptic vesicles in presynaptic terminal
Release
Depolarization of presynaptic terminal by arriving AP opens voltage-gated Ca2+ channels, Ca2+ influx triggers fusion of vesicles with presynaptic membrane, release of NT into synaptic cleft
Receptor binding and cellular response
NT molecules bind to receptors on membrane surfaces, either on postsynaptic cell or presynaptic autoreceptors
Postsynaptic receptors: usually open more channels which may lead to EPSPs or IPSPs
Autoreceptors: modulation of NT synthesis and/or NT release
Inactivation
Enzymatic degradation of NT, uptake of NT by the presynaptic neuron or glia
Role of Ca2+ in neurotransmitter release
Triggers the release of synaptic vesicles containing NT into the synaptic cleft
Research questions from the lab
Both selective muscarinic and nicotinic antagonists produced a change in contraction response
Addition of 5-HT resulted in change in frequency
Serotonin receptors are inhibitory, addition of agonist for seratonergic receptors resulted in decreased contraction frequency
ACh-Rs
Nicotinic
Ionotropic
Acted on by ACh and nicotine
Muscarinic
GPCR
Acted on by ACh and muscarine
Drugs
Agonists
Direct
Bind to the receptor itself
Indirect
Affect the action of the NT: facilitate synthesis and release, prevent NT degradation
Antagonists
Direct
Bind to the receptor itself, preventing the NT or agonist from binding and inducing the normal response
Indirect
Interfere with the NT activity: decrease NT synthesis and release, enhance NT degradation
Non-selective agents
Bind only to one receptor subtype for that neurotransmitter
Ex. ACh is a non-selective agonist for all ACh-Rs because it acts on all of them regardless of subtype
Selective agents
Bind to all receptor subtypes for that neurotransmitter
Interpretation of muscle contraction traces
Larger individual contractions = larger amplitudes
Increased total contraction = upward baseline shift
Doesn't relax back to original baseline
How an antagonist can have an excitatory effect on a neuron
Inhibiting an inhibitory input results in an excitatory effect on the postsynaptic neuron
Calculate % change in contraction amplitude and frequency
Change in amplitude
[(A-B) x 100] / B
A = average of 4 contractions' amplitudes immediately after drug application
B = average of 4 contractions' amplitudes immediate before drug application
Amplitude measured from bottom of trace before drug to tops of peaks of interest (either before or after drug addition)
Change in frequency
[(Fa - Fb) X 100] / B
Fa = frequency of first 4 contractions immediately after drug application
B = frequency of first 4 contractions immediately before drug administration
Frequency measured in contractions/min
Lab 9: EEG
Noninvasive techniques
Structural info
CAT
Cranial axial tomography
MRI
Magnetic resonance imaging
DTI
Diffusion tensor signaling
Functional info
fMRI
Functional magnetic resonance imaging
EEG
Electroencephalography
PET
Positron emission tomography
EEG
Strengths
Good temporal resolution
Does not require surgery, breaking of tissue
Limitations
Poor spatial resolution; activity from thousands of neurons at once
Cannot differentiate excitatory from inhibitory APs
Poor signal-to-noise ratio
Characteristics
Reflects sum of APs from cortical nearby the electrodes
Electrodes placed against the scalp
Proposed polysomnography experiment
EEG
Measure brain activity
EOG
Measure eye movements
EMG
Measure muscle activity
GSR
Measure arousal
Measure of activation of the sympathetic nervous system
Increased perspiration
Increased skin conductance
EKG
Measure heart activity
Sleep
Deprivation
Major cognitive deficits
Psychosis, impaired cognition, irritability, impaired memory
Rebound
Stage 3 delta
More time in Stage 3, get to Stage 3 quicker
REM
More time in REM, get to REM quicker
Progression
As sleep deepens, sleep waves become more synchronous, higher amplitude, and lower frequency
Beta to alpha to theta to delta waves
Reflects a shift from cells firing sporadically to firing simultaneously
Sleep stages
Stage 2
Increasing % synchrony, sleep spindles, and K-complexes
Stage 3/4
Delta waves
Stage 1
Increasing % of alpha and theta waves
REM
Resembles wakefulness, with beta and theta waves
Inactive muscles, rapid eye movements
Awake
Asynchrony, beta waves
Active muscles, eye blinks
Wave types
Alpha
Relaxed and drowsy
Theta
Light sleep (central midline)
Awake and concentrating (temporal cortex)
Beta
Largest frequency
Awake and alert
Delta
Smallest frequency
Deep sleep