FinalN158

Neurotransmitter

Adrenaline

Noradrenaline: neurotransmitter

Limbic system: essential for emotional learning and expression. Also modulates memory consolidation by emotional state

Drug inhibiting a neurotransmitter by slowing its release, production, or persistence. May block receptors of the neurotransmitter

D-2-amino-5-phosponovalerate. antagonist of NMDA receptors

Forebrain components of the extra pyramidal motor system including the striatum

Changes in synaptic efficacy due to memory formation

Hebb's notion of a local circuit of connected neurons that develop to represent a specific precept or concept

Major structure of the brain stem involved in motor control. Critical for skeletal muscle responses

Systematic representation of topology in the brain

Functional and anatomical organization in the cortex. Similar functioning cells are arranged vertically across layers in parallel columns

Nonspatial learning: learning guided by a stimulus

Learning guided by the use of spatial relations among external stimuli

Everyday facts or information includes both episodic and semantic information

Damage in A but not B results in failure in task X but not Y. Damage in B but not in A results in failure in task Y but not X

Position in environment relative to the orientation of the body ex left or right

Memory expression based on conscious memory recollection

Representation of life experiences requires conscious recollection

• Connects hippocampus with other hypothalamus thalamus septum and brain stem
• Modulates arousal and consolidation

Unconscious changes in performance due to previous experiences

Contains Ammons horn( ca1 and ca3) dentate gyrus and subiculum

Emotional circuits in the brain including the amygdala septum and prefrontal cortex and areas of the mid brain

Neurotransmitter receptor found in post synaptic elements and allow charged molecules (ions) to flow

Do not open channels and doesn�t directly affect the membrane potential but tend to have longer lasting effects

• Facilitation or retardation of memory consolidation mediated by hormones
• Adrenaline via vagus nerve to the amygdala is most relating to emotional memory

• Subcortical structure of the forebrain contains the caudate and putamen
• Critical for habit memory due to functions in the extra pyramidal motor system

Ones body of world knowledge and organization of memory

Position in environment independent of orientation or location of subject

• Showed first double dissociation experiment showed cognitive map vs habit
• Rotated the T-Maze experiment.
• Found that regularly trained rats used a "cognitive map" and Overtrained rats practiced "habit"

Found that some cells react to a specific place and a specific intention. Cells in rats in T-maze react to intersection and turning left, but not turning right

Rotated T-maze showed early signs of multiple types of learning my observing place vs response in rats

Selective bilateral calcification of the amygdala but not the hippocampus

• Due to damage in neocortex
• 1 category of amnesia and rest of memory is fine

Both created and stored in the neocortex but requires hippocampus for consolidation

• Typical example
• Brain categorizes information and conforms it into an archetype aka stereotype

• Used the subtraction method to look for brain activity while naming things in two trials for two categories
• Found separate brain real estate for each category

Can�t recognize faces

In temporal cortex cares about particular faces and only responds to specific aspect of the face

• One cell for one memory
• Jk hypothesis

• Rat Hilton
• Examined bushiness of dendrites in parallel fibers in cerebellar cortex and increased synapses to Purkinje cells

• Main cells in cerebellar cortex
• Sends inhibitory inputs to deep nuclei

• Excitatory inputs for Purkinje cells but work indirectly
• Originates from brain stem nuclei and run via parallel granule cells perpendicular to the Purkinje cells

• Another excitatory input to the Purkinje cells
• Originates from the inferior olivary nucleus of the medulla
• Wraps around cell body of Purkinje cell with all or nothing influence

• Long term decrease in synaptic activity can last for multiple hours
• Discovered by Ito

• Central for cerebellum contribution of motor learning
• Equals inhibition of Purkinje cells = no inhibition of interpositus

• Bottom of cerebellum vital for motor learning
• Activates red nucleus

• Required for blinking circuitry
• Without = no learning
• With = instant learning

Tone puff eye blink reflex learning

Tone => auditory nuclei=> pontine nuclei=> mossy fibers => cerebellar cortex (purkinje cells) =| interpositus

Puff=> trigminal nucleus=> inferior olive=> climbing fibers=> cerebellar cortex (purkinje cells)=| interpositus

Together activate LTD when mossy and climbing fibers work together

Interpositus => red nucleus => cranial motor nuclei=> blink ( UR + CR).

Conditioned response goes away when paired stimulus is unpaired

Vital for tone + puff learning. Without it rabbits showed extinction when conditioned stimulus is still paired.

Memories need some time before becoming fixed

Usually due to trauma. Cannot recall information prior to traumatic event

Cannot recall information following trauma.

• 1) tone/puff unpaired
• 2) tone+puff paired
• 3) test with subtraction logic
• Conclusion: people with cerebellum damage don�t learn reflex as well

• Random image pairing. Initially 1 neuron only cares about 1 image. After pairing 1 neuron cares about 2 images.
• Studied the ventral visual stream. STM vision and LTM storage

Whats what

Whats where

STM from neocortex=> hippocampus=> LTM in neocortex

Somatosensory cortex has plastic neurons due to experiences

Homunculus aka brain real estate for sensory info

• Does the auditory cortex learn?
• Experiment does tuning curve of an auditory cell shift.
• 1) find cell of best frequency
• 2) Pavlovian conditioning: foot shock paired with neighboring frequencies
• 3) find cell again

Auditory cells are tuned to a specific frequency and best respond to one frequency

Sensory cortex couldn�t learn because basic sensory function doesn�t change

Shift does appear with conditioning. However hippocampus vital for recall. Tuning curve will unshift the next day if hippocampus is destroyed.

Muscle memory and habit

• Visual vs spatial discrimination
• 1) see ball get on ball at fixed spot
• 2) go to same spot with hidden ball
• 3) go to seen ball in new spot
• Results: control goes to new ball. No hippocampus goes to new ball. No striatum go to hidden ball.

• Triple Disociation Test
• Focused on the striatum, hippocampus, and amygdala.
• Showed triple disociation with rats in a radial maze given various training

• 1) set of cards correlate with sun or rain. Cards not perfect correlation but probability.
• 2) not conscious learning, not declarative memory recall
• 3) stimulus and response learning

• Parkinson�s = no SR learning
• HM/ CAS = normal learning
• When asked about test after
• Parkinson�s = normal recall
• HM/ CAS = fail to recall
• Shows double dissociation!

• Monkeys trained on specific sequences of light
• SR learning: specific sequence of light = get juice
• Cell responds to L light only after U light appears
• Cell responds to particular part of sequence
• Cells in striatum respond to robot SR

Skill learning, priming, and conditioning aka nonconscious learning

Muscle memory mostly in basal ganglia, motor cortex, and cerebellum

Cued recalling of an earlier exposure

Sensory cues like vision and perception works mostly in frontal lobe

Stimulus recalls past thought reduces activity in frontal lobe

Simple delay and trace conditioning

• CS is brief and followed by a blank "trace" period then the US.
• Hippocampus and neocortex dependent

• Standard CS and US pairing
• Cerebellar circuit

• Classic amnesia syndrome = HM amnesia
• Can answer primed word completion test but not word recall tests

• Medical temporal lobe = no good for priming
• Neocortex = good for priming

• Visual cortex damage = Missing sight
• Tested for priming
• Declarative memory = fine
• Priming ability = poor

• 1) show words list a
• 2) show new words list b
• Priming = less active sensory cortex = more faster recognition = more efficient and less energy

• Students of Ebbinghaus
• 2 word list study
• Learning list 2 interrupted learning of list 1
• More time in-between learning two lists = less interruption of learning

1938 first to discover electroconvulsive shock

Electroconvulsive shock still used today for treatment of depression

1949 light+shock in one compartment. Other side safe. Rat learns active avoidance to avoid shock.

Takes about 1 hr for memory consolidation in rats. Rats with ECS don�t learn shock avoidance well. ECS has an effect like retrograde amnesia

• Why is retrograde amnesia as loss of recent memory first?
• Temporally graded memory loss occurs becuase consolidation is interrupted by truamatic event.

• Retrograde enhancement gradient: new memories = more malleable.
• Retrograde amnesia gradient: new memory = less malleable

Info gained immediately before trauma is lost, but info gained longer ago is retained.

After trauma the enhancement of memory decreases as time goes on

After trauma new memories are most susceptible to loss.

• Explains why there is both retrograde amnesia and anterograde amnesia in patients suffering from head trauma.
• Trauma hinders both memory storage and memory recall

At the time the status quo: drug=> train/ learn=> wait => test (no distinction)

Train/ learn => drugs => wait => test. Creates distinction because drugs don�t effect learning or recall phase, only consolidation phase

Rat poison used in a really small dose to enhance memory

McGaugh discovered the right drug at right dose enhances memory and performance. Too little or too much drug inhibits memory/ performance

Stimulants = amphetamines = catechamines = fight or flight hormones in adrenal glands.

Adrenal hormone = adrenaline and Norepinephrine ( in brain)

An endogenous morphine naturally exists in body

Soldiers given morphine within two hrs of injury are less likely to get PTSD

Opiate used to numb severe pain by acting in the central nervous system

Post traumatic stress disorder an extremely painful memory never goes away and inhibits daily life.

• 1) adrenaline activates the vagus nerve
• 2) adrenaline and glucose work together to activate the amygdala

Triggered by stressful situation. Stress activates adrenal glands. Adrenaline goes through blood stream to vagus nerve. In the brain Norepinephrine also activates vagus nerve. Vagus nerve regulates heart rate.

• Adrenaline
• Adds lots of glucose into the blood stream during stress. Body uses sugar to run or fight.

• Aka nucleus tractus solitarii
• Connects the vagus nerve in the medulla to the amygdala

Numbing drug which renders part of the brain useless

Yes. Test with lidocaine in NTS => train/ learn=> drug = memory loss ( in rats with enhanced memory

NTS activated by Norepinephrine. Norepinephrine stimulates the brain to enhance memory. No NTS = regular memory

Inhibits Norepinephrine receptors. Blocks memory enhancing effect of Norepinephrine

MODULATES memory can either enhance or hinder

• Legion amygdala=> train=> induce adrenaline=> record = no memory enhancement.
• Measure amount of Norepinephrine present in amygdala
• Intverted U relationship for memory and dose

Shock chamber and 24 hr recall. More Norepinephrine = longer reenter time

No. Amygdala only modulates another system

Normal people remember emotional info more than neutral info. Propranolol inhibits amygdala, Propranolol subjects have almost no preference.

• Experiment: watch=> wait 3 weeks=> test memory
• Watch 2 films while in pet scan. ( men only) more glucose in amygdala = better recall

• 1. Propranolol selectively blocks emotional memory
• 2. German without amygdala = person on Propranolol
• 3. Amygdala not needed for declarative memory

• Watch film=> inject adrenaline=> wait 1 week=> Test
• Found an inverted U relationship for cortisol and memory.

• Morris Water Maze Revisted
• 2 Tests
• Training=> inject amphetamine to stimulate region=> wait 24hr => lidocaine amygdala => test
• A. Spatial test where position is constant but hidden.
• B. Cued test where positision is variable but visible.
• Results: Amphetamine in amygdala enhances performance on both tasks. Amphetamine aids in spatial task for the hippocampus, but not for cue task.
• Amphetamine aids in cue task for striatum, but not for spatial task.
• Shows double dissociation and amygdala modulates other regions of brain.

Neurotransmitter which inhibits the release of norepinephrine.

Memory helps predict the future

Stress hormone responsible for " i know it but cant remember" feeling

Has inverted U effect on memory. Depends on dose and situation. AKA MODULATION

• Men ice vs no ice = better recall with ice (increased coritsol)
• Women ice vs no ice = equal recall (despite increased cortisol)

Men and women react differently due to different brain hormones present mostly due to menstrual cycle

Hippocampus => pyramidal cells => full of cortisol and estrogen receptors

• 3 groups of women
• 1. Low estrogen/ low progesterone = early follicular stage
• 2. High estrogen/ low progesterone= late follicular stage
• 3. Low estrogen/ high progesterone = mid flutor stage
• Group 1 neutral recall
• Group 2 decrease recall
• Group 3 increase recall as more cortisol enters brain
• Why? Unknown

• Men use right amygdala recall mostly the gist
• Women use left amygdala recall mostly the details

Propranolol ( beta blocker) reduces the gist memory in men and reduces the details memory in women.

• Normal cycling women recall details of emotional scene best
• Normal men recall gist of emotional scene best
• Oral contraceptive women recall gist of emotional scene best ( at like men)
• Shows that social norms are not an influence

Science: women = men + ~ estrogen

Epilepsy. Removed hippocampus and amygdala. Defines CAS.

Medial temporal lobe main region causing temporally graded memory loss

Why is retrograde amnesia as loss of recent memory first?

• Retrograde enhancement gradient: new memories = more malleable.
• Retrograde amnesia gradient: new memory = less malleable

Info gained immediately before trauma is lost, but info gained longer ago is retained.

After trauma the enhancement of memory decreases as time goes on

After trauma new memories are most subceptible to loss.

• Explains why there is both retrograde amnesia and anterograde amnesia in patients suffering from head trauma.
• Trauma hinders both memory storage and memory recall

Organ of common sense

Synaptic junction where ions flow from post to pre mostly ion gated

Brains ability to adapt and be fluid

Active construction project

Memory disorder inability to recall

MRI FMRI EEG MEG electrical recording animal research

• Connection: cajal
• Cognition: james
• Compartmentalization: james
• Cognition: james

Found that brain is not symmetrical. Came up with idea of zones in the brain

"form reflects function" not really in brain

• Cajal
• 1. Brain is made of neurons
• 2. Law of polarization: neurons are unidirectional

Golgi mesh theory wrong!

Interactive action of the nervous system. Coined the phrase synapse

• Nonsense syllables and learning.
• Quantified learning with the unit "savings"
• savings = retention in terms of reduction of learning trials
• 1. Forgetting is non linear
• 2. Distributed is better than mass practice (cramming)

• Loss of memory is inversely related to the time elapsed between event and injury.
• Memories need a certain time to be organized and fixed

Memories at the highest level of analysis. Psychological level

Memory is stored throughout the brain but regions are organized to certain info

Memory needs time to be stored and fixed

Neurons connect brain circuitry to body

Conditioned reflex aka SR

I robot SR Thorndike puzzle boxes anticognition

I think cognition James principles of psychology

Memory degradation

Little consolidation of info common in alcoholics

Learning is a gradual connection of sr

Ca+2 determines length of action potential

• Metabotropic receptor
• Serotononin => ATP=> cAMP=> PKA=| K+

Opens ion gated receptors to Na+ to flow in cell and K+ out

Fewer neurotransmitters released from the post synaptic junction to the next neuron

Regulates Ca+2 flow

• Glutamate =>Mg+ leaves NMDA receptor=>Ca+2 flows in
• Ca+2 => cAMP=> PKA=> close K+ channels

Serotonin=> ATP=> cAMP=> PKA => nucleus=> CREB1

Activated by MAPK

May inhibit creb1 and activate creb2.

Long term potentiation: long lasting epsp. A permanent increase in synaptic efficiency

Sea slug

Reinforcement enhances sr connection aka learning

Nonlinear learning a sudden flash of insight.

Animals can elastically use a cognitive map to efficiently go around detours

• Schema power to remember. Experiment:
• 1. Story about indians
• 2. Measure content obtained
• Result: memory is a reconstructive process (not regurgitation.

An organization of information in the mind

Neurons receive same input but sends out less neurotransmitters (desensitize)

Break the habit by adding a new stimulus

• Gill redrawal reflex in aplysia.
• Sensory neuron sends instructions to motor neuron via a ganglion L7.

Sensory neurons receive the same input but sends out more neurotransmitters to the motor neuron to get an enhanced reaction

Creb-antisense = blocks creb1. Used a cannula to inject creb antisense into hippocampus. Result: blocked long term memory formation

Discovered LTP. Gave a tetanus zap to neuron to create a long lasting action potential

• 1 prominent in the hippocampus
• 2 develops rapidly
• 3 lasts long hours
• 4 synaptic specificity
• 5 associative
• 6 theta rhythm

• Larson and lynch
• Hippocampus as oscillating theta rhythm used to navigate the world

AP5 blocks NMDA receptor. No effect on EPSPs.

• Regulates neurotransmittance in the hippocampus
• Allows Na+ and K+, but no Ca+2 to flow more easily.

• Water maze task. Rats with hippocampal damage must find a fixed hidden platform.
• AP5 definitely hinders performance by numbing the hippocampus but doesn�t effect all memory

SR learning is the only type of learning at its like a chain link fence

• 1. Sharpening learning
• 2. Additions and omissions
• 3. Normalization/ rationalization

Researches false memory at UCI.studies bartlettization of memoryConcludes that certain cues and induce a false memory hence "leading the witness" is big problem

Classic Amnesia Syndrome famous patients HM and IS

• 1. Intact LTM
• 2. Intact STM
• 3. Intact sensation and motor function
• 4. Intact intelligence
• Cannot consolidate STM to LTM

• Removal of hippocampus, amygdala, and some of the surrounding cortex due to severe epilepsy.
• After surgery severe anterograde amnesia. Could not consolidate new memories, best recollection of childhood memories.
• Intact motor function and intelligence. Capable of very short term memory.

Damage to Amgydala ONLY. Not CAS declarative memory is just fine. A bit emotionally insensitive.

• Severe damage to parts of the hippocampus
• NOT a CAS patient
• Still was able to recall fragmented memories
• Bits of the hippocampus worked to form broken memories

• Virus destroyed hippocampus surrounding cortex and the amygdala
• CAS symptoms
• Has LTM and STM
• Motor function and intelligence are fine
• Cannot consolidate new memories
• No declarative or conscious memory recall
• Yes procedural and emotional memory

• Stroke destroyed CA1 layer of hippocampus
• 50% CAS symptoms
• Had LTM temporally graded amnesia motor function but a broken consolidation circuit

• Ammons Horn ( CA1&CA3) the dentate gyrus and the subiculum
• Pryamidal cells in Ammons Horn are interwoven with mossy fibers in dentate gyrus. Information flows to subiculum through the fornix to other areas of the brain.

• 1. Train for ab and xy pairs
• 2. Train for bc and yz pairs
• 3. Test for ac and xz pairs aka transitivity
• 4. Test for cb and zy pairs aka symmetry
• Result: Normal rats could transfer info. Hippocampal damage rats could not.
• Normal rats could do symmetry. Hippocampal damage rats could barely do it.

• Subject must remember a stimulus after a delayed period without the aide of cues. Three phases:
• 1. Sample phase: view the stimulus cant respond
• 2. Delay phase: stimulus cannot be seen
• 3. Choice phase: subject must select an alternative stimulus to earn a reward

• For DNMS and Delayed response, normal monkeys did much better than HM monkeys.
• For barrier motor skill task and lifesaver motor skill tasks, normal and HM monkeys had the same results

Main culprit in CAS not just the hippocampus

Positron emission topography. Inject radioactive glucose into blood use PET to get image

• Stimulation (test) - control (normal brain activity) = difference.
• Worked for vision and visual cortex.

Subtraction logical fails if the structure is always active. Hippocampus never stops working.

Has lots of variability so data must be normalized for analysis.

Compare images while learning with images a day later

• 1. Subject listens to a list of words
• 2. Wait 24 hours
• 3. Free verbalized recall of list
• Result: more active hippocampus = more memory

Functional magnetic resonance imaging based on amount of oxygenated hemoglobin in blood

• Test: scan pics=> wait 24 hrs=> test memory
• Results: Those who remember have a bigger BOLD response then those who forget.