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PSYC210 Exam 1

by: Yiyi Wang
Yiyi Wang

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These notes cover everything in class up to exam 1 with Professor Galvez
Intro to Behavioral Neuroscience
Class Notes
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Popular in Intro to Behavioral Neuroscience

Popular in Psychology (PSYC)

This 14 page Class Notes was uploaded by Yiyi Wang on Wednesday September 14, 2016. The Class Notes belongs to PSYC210 at University of Illinois at Urbana-Champaign taught by Galvez in Fall 2016. Since its upload, it has received 5 views. For similar materials see Intro to Behavioral Neuroscience in Psychology (PSYC) at University of Illinois at Urbana-Champaign.


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Date Created: 09/14/16
PSYC210:  Nervous System:  Two primary cell types: Neurons & Glial  Central Nervous System  Spinal cord & brain  Generally, does not regenerate  Exceptions: glial cells (reproduce), some neurons  Peripheral Nervous system  Regenerates after damage  Divided into two parts:  Sematic: Voluntary muscles  Autonomic-involuntary  Sympathetic- fight or flight (stress)-prepares for action  All spinal fluid, primarily Lumbar, and Thoracic  Parasympathetic- regulation of internal organs –prepares body for restoration and relaxation  Three nerves: Ocularmotor nerve, Vagus nerve, Facial nerve, Sacral Portion  Damage of Sacral region would not damage sympathetic nervous system  Brain Membranes  Several layers of coating and covering for protection  Skull, three Membranes that surround brain and spinal chord  Dura Mater (tough Mother)  Sack that covers the brain and spinal cord  Keeps cerebrospinal fluid in  Arachnoid Mater  Web-like fiber that helps regulate the cerebral spinal fluid  Helps control how much cerebral spinal fluid is actually produced  Pia Mater (Tender Mother)  Covers and protects the brain  Only membrane that extends into the folds on your brain  Cerebral Ventricles: (typically hollow, filled with cerebral spinal fluid)  Lateral Ventricles- one on each side of brain  Third Ventricle-  Fourth Ventricle-  Choroid Plexus: Makes cerebral spinal fluid, red line that goes in the inside border  Big Brain- Small Skull  Surface area of neocortex is about the size of the pillow case, so it’s crumpled up to make it fit in the skull, which creates all the folds and crevices of the brain  Gyrus (Gyri)-hills  Fissures or Sulcus (Sulci)- valley  Neocortex is the outer shell of the brain, divided into two halves by the longitudinal fissure  The right half of the brain processes information for the left half of the sensory world (vice versa)  Regions of the brain:  Frontal Lobe (planning), Parietal Lobe (sensory), Temporal Lobe (auditory), Occipital Lobe (vision)  Occipital Lobe “what” pathway of visual stimuli is processed into the Temporal lobe, “where” pathway of visual stimuli is processed into the Parietal Lobe  Broca’s Area (part of frontal Lobe)  Precentral Gyrus (Movement) (Part of Frontal Lobe), Postcentral Gyrus (deals with touch or somato-sensory) (part of parietal lobe)  Central Sulcus  Sylvian Fissure- separating the frontal lobe and the parietal lobe, above the temporal lobe  Olfactory Bulb- deal with olfaction (odor stimuli)  Hindbrain: Pons, Medulla, Cerebellum  Optic Chiasm, Pituitary, Mammillary Body  Cingulate Gyrus (underneath frontal lobe)  Forebrain: Thalamas, Hyperthalamus, Cortex, Hippocampus etc. (everything else)  Corpus Callosum- Axon fibers that send signals from one side of the brain to the other side  Pineal Gland  Midbrain: Interior Colliculus, Superior Colliculus, Tegmentum, Periaqueductal Gray  Fornix  Basal Ganglia: response learning addiction, motor processing  Hippocampus: limbic system (group of structures that are connected that deal with learning and memory), place learning, binding (associative component)  Anatomical Direction  Anterior (Rostral) (Front)  Posterior (Caudal)(Back)  Dorsal (upper)  Ventral (lower)  Orientation changes when you get to the spinal cord because we are two-legged creatures  Back becomes Dorsal surface  Cells in the in the Nervous System  Neurons (100-150 billion)-semi-permeable membrane: can allow ions to pass through, but only certain ones (selective)  Polarized cell, not at 0 mV  Glial Cells: supporting cells, form a barrier between blood and brain (blood/brain barrier)  How Neurons work: a x o n + b o d y a x o n t e r m i n a l s N a a x o n   h i l l o c k + K  I n p u t   o n e C o n d u c t n gu t p ount eo n e  InL i g a n d ­ g a t   c hol tna ng ee l­sg a t e d   c h a n n e l shannels): Cell body, dendrites  Conducting Zone: (voltage gated channels-channels that open depending on the internal voltage of the cell): Axon  Output Zone (both voltage and ligand channels): Axon Terminals then synapsing onto dendrites of a another neuron  Types of Neurons  Multipolar Neuron: cell body is in input zone with multiple branches coming out of cell body  Bipolar Neuron: cell body is conducting zone with two branches (processes) coming out of cell body  Monopolar Neuron: cell body is in conducting zone with one branch (process) coming out of cell body splits where all of it is in conducting zone and comes out into the input zone  Portion that comes out into the input zone is the dendrite processes that receives sensory information  How Electrical Signaling Works:  Outside of cell has high Sodium concentration  Inside cell has high potassium concentration  Cells work very hard to keep that the case  How cells communicate or activated or inhibited with each other is change in (voltage) electrical current in either side of cell  Way to change voltage is changing relative concentrations Sodium and potassium on either side of cell  Resting Potential: Through use of sodium potassium pumps that keeps appropriate concentrations of sodium out of potassium in (-60 to-70 mV)  Action Potential: taking resting potential and changing Sodium and Potassium concentration and changing internal membrane potential of the cell,  generates a current down the axon and when it reaches the axon terminal, it can then stimulate the next cell with either excitatory current, or inhibitory current, depending on what’s being released, and what receptors are on that side  1. Resting state-little bit of activation, more Na outside, more K inside, influx of Na into the cell causing a depolarization  2. Depolarization-increase mV potential in the cell, if it gets over the threshold potential, it’s going to activate two voltage-gated channels Na & K (both Voltage-gated channels)  Na channels=fast, K=slow  3. Rising phase of Action potential-Na flowing in, potential going up, when it reaches top, K channels start to open (30 mV)  4. Falling Phase of Action Potential- K wants to get away from the cell, flowing out of the cell, because it’s positively charge, potential starts going down  5. Undershoot-The channels open and close slowly, therefore, when the potassium channels start to close, they don’t really close up until the potential has already dipped below resting state  Na/K pumps start working to get it back to resting state -60/-70 mV  Electrical current flows through and activates sodium and potassium channels next to it, generating multiple action potentials through the axon  Reaches Axon terminal, stimulating the release of a chemical—neurotransmitter  Neurotransmitters are going to bind onto the ligand-gated receptors on some dendrite  Sodium can flow through the ligand-gated receptor into the dendrite, it’s going to depolarize that dendrite, moving the resting potential up, but electrical current will slowly go down due to resistence (graded potential-passive flow of current through the structure (dendrites or cell body))  Generates a current down axon, when reaches axon terminal, it get excited  Excitatory Postsynaptic Potential (EPSP)-Na (positively charged) into dendrites, exciting the neuron  Inhibitory Postsynaptic Potential (IPSP)-Cl (negatively charged) into dendrites, inhibiting the neuron  As the action potential is conducted along the axon, the potential does not change in size or shape  Mediated by how fast the Sodium or Potassium channels open or close, which is always the same  This is because the potential is regenerated at each point along the axon  Graded potential-No regeneration, potential decreases=graded conduction  Regeneration of Action Potential  After reaching the threshold Na+ enters through the voltage-gated channels  The entry of Na+ causes the membrane potential to reach +30mV  Positive charge spreads throughout the membrane, depolarizes adjacent parts and process repeats  Membrane depolarization opens voltage-gated Na+ channels and Na enters the neuron  The spread of charge depolarizes adjacent points long the membrane, opens voltage-gated channels, Na+ enters, etc.  Backward spread of charge does not open voltage-gated Na+ channels because these channels not close they inactive!  Refractory Period  Each channel has its own refractory period  Absolute refractory period:  Lasts 1 msec  Sodium channels closed and inactivated, so the neuron will not generate another action potential  Limits neuron to a maximum of 1000 action potentials per second  Relative refractory period (after absolute)  Lasts 3-4msec  Hard to generate action potential, but possible  Conduction Velocity  Action Potential: slow (10 meters per second) conduction of action potential along unmyelinated axon  Speed of conduction in uninsulated avon varies from .1 meter/second to 35 meters/second-depends on axonal thickness  Thick axon-fast conduction, more charge carriers (ions)  Thin axon- slow conduction, fewer charge carriers  Salutatory Conduction in Myelinated Axons-speeds up action potentials  The longer distance of neuron signal, has to be myelinated to speed up neuron conduction (brain to big toe) but shorter distance, neurons doesn’t need to be myelinated (within frontal lobe)  Many axon are insulated by myelin, which is made be Schwann cells in the peripheral nervous system and oiligodendrocytes in the central nervous  Myelinated portion of axon-graded potential  Nodes of Ranvier- portion of axon that is not myelinated and action potentials pass through  Current flows to the next Node of Ranvier so the action potential “jumps” from node to node (saltatory conduction)  Action potential can fail at two nodes and still be regenerated  Speed of salutatory conduction is up to 120 meter/secs (4 times than unmyelinated axons)  Two Types of Synapses:  Chemical Synapse (most common)  Terminal filled with vesicles that release chemicals (neurotransmitters) onto the receptors on the post-synaptic side in a neighboring dendrite of another cell  Synaptic delay (~1ms)- time for vesicle to bind to the membrane, neurotransmitter to be released, then diffuse across cleft, then bind to ligand-mediated receptors on post-synaptic side  Cells can do things to modify this (shorter or longer), but on avg just 1 ms  Proteins made at Cell body, they need to get to the axon terminal  Dendric Exspine: on the dendrites themselves, there are protrusions that will come out and these will be the sites of connections, increases surface area  Neurotransmitter manufactured in cell body by ribosomes along with rough endoplasmic reticulum (ER)-properly folded up, folded layers of membrane where proteins are assembled  Moved by smooth ER to Golgi apparatus and packaged into synaptic vesicles in the cell body  Microtubules transport synaptic vesicles (and other material including enzymes that can synthesize neurotransmitters) down the axon to the synaptic terminal  Offers an anchor to transport the synaptic vesicles to the synaptic terminal  1. Action potential invades synaptic terminal  2. Open voltage-gated calcium channels enters the terminal  depolarization that comes down to the axon terminal will open these channels that’ll allow Ca2+ to flow in the axon terminal  3. Ca2+ causes (stimulates) synaptic vesicles to bind to presynaptic membrane  4. Vesicles burst open and release contents into synaptic cleft  5. Neurotransmitter diffuses across cleft and binds to receptors on post- synaptic side  6. Neurotransmitter becomes unbound  Reuptake neurotransmitters on pre-synaptic terminal into vesicles  Removal from synaptic cleft (Glial cells removes it)  Electrical Synapse (not very common)  Tight Junction; proteins actually span across the membrane  Fast/no synaptic cleft (no space between the pre and the post synaptic terminal, between the two cells, smashed up against each other)  Ions and electrical chargers are allowed to flow freely from one side to the other  Electrical potential travels directly to next neuron  Two types of Receptors  Ionotropic receptor (ligand-gated ion channel, fast)  1. Neurotransmitter binds directly to the channel protein  receptor goes through a confirmation change, allowed ions to flow in  2. Channel opens immediately  Ions flow across membrane for a brief time  Metabotropic receptor (G-protein-coupled receptor, slow)  1. Neurotransmitter binds G protein-coupled receptor (goes through a confirmation change)  2a. G protein activated which then goes on to do something else  2b. In this case, activated G protein subunit moves (binds) to adjacent (receptor) ion channel, allowing receptor to open allowing ions to flow in, which causes a brief delay  3. Channel opens, open flow across membrane for a longer period of time  Offers an extra level of control  Synaptic Transmission  Neurotransmitter acts on receptor at ligand-gated channels to produce an EPSP or IPSP  Receptor can be coupled to ion channel=ionotropic (fast acting)  Receptor may be coupled to a protein (G-protein)=metabotropic (slower because part of the protein breaks off and changes a function within the cell release Ca2+ from intracellular (internal) store)  Two major neurotransmitters:  Glutamate (EPSP)  GABA (IPSP): cannot get an action potential, dampens the cell Touch  Somatosensory System: Relays information about the body  Touch, Temperature, Body Position=proprioception, Organic senses (heartburn), Pain (nociception)  Labeled Line System  Receptors=neurons that transduce or change a physical stimulus into neural events  In the skin, each receptor has a specialized ending that responds to a specific attribute (type) of the (sensory) stimuli  Labeled Line= different receptors for different qualities have different lines to the brain  Free nerve endings (pain and temperature)- epidermis –top of your skin  4 touch receptors that deal with different types of touch stimuli  Vibration (Pacinian corpuscle)- large blue areas (fast adaption)  Not very important if someone is vibrating hand  Touch (Meissner s corpuscle)- small, sharp boundaries (fast adaptation)  Touch (Merkel s discs)- small, sharp boundaries (slow adaptation)  Stretch (Ruffini s ending)- large blue areas (slow adaptation)  Receptor fields: where do these different types of receptors respond  Blue area=area that it receives sensory stimulation from  Purple dot= receptor itself  Adaptation=loss (change) of sensitivity to continuous presence of stimulus  Manifest in a loss for somatosensory  Receptors tells brain initial stimulation activation and then stops. There’s no reason for receptors to keep telling brain that it’s still there, nothing’s changed, wasted information  Soon as you change stimulation, then it tells the brain  Receptor Potential  A Pocinian corpuscle respond to vibration  When deformed (skin vibrated), sodium channels are opened (stretched), which depolarizes the ending  If ending depolarized enough, produce an action potential  Receptive Fields  Each receptor has a receptive field=the region of the receptor surface that excites or inhibits a sensory neuron  Size of receptive fields: For each type of receptor, the receptive fields are smallest in the fingertips, larger in the hand, even larger in the arm  Varies with use  Somatosensory Pathways: Information ascends from the dorsal root to the dorsal columns to the medulla, crosses over to opposite side of the brain, goes up the medial lemniscus, then to thalamas and then to somatosensory cortex (parietal lobe)  Dermatomes: An area of skin that is mainly supplied by a single spinal nerve  Spinal cord regions bottom-up: Sacral, Lumbar, Thoracic, Cervical  Damage to the spinal cord goes everything down (ex. Damage to Cervical region, everything under it is damaged)  Somatosensory Cortex: posterior to the central sulcus (post-central gyrus)  How much area in your somatosensory cortex (cortical landscape) is devoted each part of the body (large hands=takes up large region in somatosensory cortex, small feet=takes up large region in somatosensory cortex)  Primates fingers=digits in somatotopic map  How plastic is this system? Can this system change?  Modulation of Somatosensory Representation-experiment  Mapped out location in somatosensory of different digits in monkey’s hands  He removed one of the digits (amputated one of the fingers)  When damaged, digits merge together to make up that missing area  Does cortical reorganization only happen in extreme situation? (learning a new subject, language) No.  Trained monkeys to keep their fingers on a rotating disk with a texture (sandpaper) so they can feel the bumps passing over their fingertips  If they kept their fingers on the rotating disk for a certain amount of time, they got food reward  Receptive fields did change before and after, but the results weren’t quantified  Receptors on fingers are going through changes, they start transmitting more precise information to your brain  Developed more cortical areas dedicated to processing information in that particular region  Receptive fields, not stagnant, constantly changing depending on environment  Muscle Receptors:  Two types:  Golgi tendon organs (contraction)-submit whether or not the muscle gets contracted or not  Muscle spindle receptors (stretch)-more in the muscle fiber itself; sending stretch information  Two types:  Primary Sensory endings: innervate the central region of the muscle spindle  Secondary Sensory endings: innervate the thin ends of the muscle spindles  Both sending stretch information to the brain  How are Muscles activated?  Sensory information enters the spinal cord via dorsal root (dorsal portion of the spinal cord)  Motor information exits spinal cord via ventral root  Muscles receive neural input from motor neurons in the spinal cord  Spinal cord project of ventral root over the the muscles forming use motor ended plates with multiple synapses  For large motor end plates with multiple synapses  When you stimulate that one motor neuron, activate large muscle fibers  Bathing motor muscles to release neurotransmitter: acetylcholine (ACh)  Major components of Movement  3 levels of motor control:  1. Spinal cord  deals with a lot of motor movements so we can respond quickly to things and helps us not get hurt or damaged  Sensory event (stimulation) -> Spinal cord -> generate movement out  Sensory information coming through Dorsal root  Damage Dorsal portion of spinal cord, cannot feel but can still move  Then comes out of the ventral root  Damage Ventral portion of spinal cord, can’t move, but can feel  Spinal cord reflex:  Muscle A is stretched  Activate muscle spindle (dorsal root)  Synapse on motor neurons in spinal cord  Activate motor nerves for both muscle to counter the weight  Stretch reflex:  The position of the muscle is set by the brain  The tap on the patella tendon creates an error and the error signal to try to return the limp to its original position (doctor taps kneecap)  Fooling our nervous system into thinking we’re being stretched into a dangerous position, so activation coming out of ventral root and causes leg goes flying up  Testing neuronal pathway in spinal cord  All this happens without brain paying attention  Flexion Reflex:  If touch something hot, pain receptors will synapse with motor neurons and activating and causes hand to contract away  This happens before you know you’re feeling pain  Babinski Sign:  When you stroke the foot, baby’s foot would extend and fan out toes rather than contract like most adults would  Underdeveloped motor system  Consistent with damage to (in adults):  Motor cortex  Corticospinal track  2. Cerebellum:  Basic Coordination of limbs  regulating motor output  Eye movement, Balance, Muscle Tone  Provides smooth coordinated body movements  Receives/integrates sensory and motor information  Molecular Layer, Purkinje cell layer, Granular layer  Inputs: Climbing fiber, mossy fiber  Climbing fiber: form many synaptic connections with 1-10 purkinje cells  All the way up to the molecular layer  Wraps itself around the dendrites of purkinje cells (1-10 purkinje cells) making multiple synaptic contacts  Induce a very large depolarization to the purkinje cell causing an action potential  Mossy Fiber: Form synaptic contact with many granule cells  Granule cells (in Granular layer): project into molecular layer and form long, lateral, parallel fibers  Parallel fibers: long lateral projections that form synaptic contacts with multiple purkinje cells  As it’s passing through the dendritic tree, it’s gonna make a few synaptic contacts with the dendrites for each purkinje cell  Very large effect in many purkinje but small input in purkinje area  Not a huge effect on any one purkinje cell  Output: purkinje cell  Purkinje cell (in Purkinje layer)  Form large planar dendritic trees (flat) in molecular layer  Goes through the granular layer  Guides movements by inhibiting neurons  Sends dendrites up to molecular layer  3 functional components:  Flocculonodular Lobe: Vestibular control  Vermis & Anterior Lobe: Motor coordination, Limb Control  Posterior Lobe: Initiation/planning, Timing  Damage:  Behavioral traits: Depends upon the region damaged  Balance/gait (walking)  Guided movements  Error in range and force and movement  Inability to rapidly stop the limb  3. Cerebral Cortex  Motor Cortex:  Ventral corticopinal tract  Primary Motor Cortex (a little bit of planning)  Lesions cause weakness  Recorded neuronal activity in primary motor cortex while monkeys make arm movements  Raster plots: every time cell fires an action potential, plots a tick mark. Each row is an individual trial/experiment  When monkey turns its arm in a full circle, but neuron only fires during half the circle  But in the other direction, another different cell would be active, so primary motor cortex mediates direction  Neurons encode direction and force  Neurons fire before movement begins  Supplementary Motor area (planning movements, as soon as animal engages in motor movement, it turns off) & Premotor cortex (planning and control (execution) of limb movements)  Lesion results in loss of voluntarily movement  Recorded neuronal activity while monkey moved arm toward an object  Task:  See object that you need to move to  See activation signal  Perform movement  These areas were primarily active during the time period when the animal saw the location it needed to move to, but prior to the go signal  Good that the brain has redundancy in tasks so areas can take over when an area is not doing its job Declarative Memory  Phrenology: attributing different bumps and petrusions on the skull to correlate with personality  No scientific basis in the slightest  First time, people started partial out maybe different areas of the brain did different things  HM: Had seizures progressively getting worse  Surgeons decided to remove hippocampus and entorhinal cortex (cortex that surrounds the hippocampus)  Landmark case study that established that hippocampus is the memory structure  Can HM form some types of memories?  Mirror-tracing task: subject simply traces an object and counts the errors  the only visual cue you have is a mirror, not your hand, so you only get a mirror reflection  Overtime, people get better with this task with rehearsal  Over the course of several trials, HM did get better, and retained his performance as days pass even though he had no recollection of ever having performed the task  Resulted in severe Amnesia-memory loss  Retrograde Amnesia: Loss of memory for the past  HM-for about 10 years (on average) before surgery  Anterograde Amnesia: Inability to form new memories  HM for a long term storage of new memories  Multiple-Trace Hypothesis of Memory: You perceive world through your senses, then goes into an area called sensory buffers, then to short term memories, then consolidation and long-term memory  Sensory Memory (buffers): Large Capacity, taking in all sensory information (time frame: 1-2 seconds)  Short-term memory: if information is a little more important, enter short-term memory  Small capacity (5-9 items-digit span (how many digits can a person keep in short term memory)  15-18 seconds + with rehearsal  Can keep information alive in short-term alive through rehearsal  HM had really good rehearsal of short-term memory  Long-term Memory:  Unlimited capacity: we haven’t seen anyone who is incapable of learning new things due to lack of capacity  Lasts indefinitely: When you forget, the memory isn’t really gone, you’ve just lost the ability to access that memory Two forms of memory:  Declarative memory: Memory for facts (hippocampus-facilitates storage of factual information)  KC: Suffered a traumatic head injury due to a traffic accident  Unable to form new memories  Cannot remember personal instances in his life (autobiographical events)  Shrunken hippocampus, Selective cortical damage  Semantic memory: (familiarity) memory of meanings, understandings, and other concept-based knowledge unrelated to specific experiences, don’t need hippocampus  KC could do  Basic of knowledge of facts and language  Who was the first present? What is a bagel?  Episodic memory (recall): Memory of autobiographical events-mediated by hippocampus  What did you eat for breakfast?  Where are these memories stored? Isn’t localized in one particular area, different activation on different parts of the brain depending on what the semantic information is  Episodic memory: Anterior prefrontal cortex, posterior cingulate cortex (PCC)  What about animal literature in declarative memory?  Most common laboratory animal is a rat, do they have declarative memories?  Morris Water Maze: rodent placed in a large tub of water with a powder that makes it opaque  Platform just below the water, rat can’t see it  Number of errors getting to the platform decreases over time  They lesioned the Fornix lesion (making hippocampus go offline)  Causes animal to never get better at the task  Place cells: have a firing pattern, they fire action potentials when the animal is in a particular location in the environment  Spatial Map Theory: internal GPS,  Fits well with animal literature, but it didn’t fit with HM or people with hippocampal damage which led  T-Maze Task:  Associative Map theory: hippocampus forms associations between stimuli  Does it fit with human literature?  Can you recall an autobiographical memory, do you have to associate yourself to the event? Yes. Cannot do episodic event without associative component.  Trace conditioning: fear conditioning where you play a tone for a rodent in a chamber before shocking them  Take it away and bring it back after some period of time  Back into the chamber, play tone again, animal associates the tone with the shock and exhibit a fear response (classical conditioning)  Can also be used with an air puff in the eye  Hippocampal dependent  Delayed non-matching to sample task: monkey is presented with a sample object. When he displaces it, he finds a pellet of food beneath  After a variable delay the monkey is presented with the original object and another object  Over a series of trials with different pairs of objects, the monkey learned that good is present under the object that differs from the sample  When Hippocampus is carefully lesioned, monkey can do task just fine  Monkeys naturally gravitate towards whatever is new and novel  Only thing you’re asking monkey is to determine whether or not they’ve seen the object before (only needs entorhinal cortex), so monkey can do this task just fine without hippocampus  Indexing theory: hippocampus forms an indexing spot of associations  idea you have a centralized location that reaches out and grabs different aspects of memory  when you form a memory, all these different aspects of memory that are stored in difference locations are being linked together through the hippocampus  bringing memories back activating an indexing spot in hippocampus that then can back-activate all the different memories associated with that particular memory  this is okay for initial events, but not good for long-term events  How do we have different memories have different salience, lasting longer?  difficulties: HM  Multi-Indexing theory: every time you form a memory, get a brand new indexing spot in hippocampus  It looks at what is getting activated the most, everything else gets quieted down  can increase the number of connections and also the salience, the strength of the connection  HM: your memories never become hippocampal independent from this theory  Did not have a complete hippocampal removal (only 2/3s were removed)  Maybe by chance, not all the indexing spots were wiped out  Standard Model of Memory Consolidation: after repeatedly activating certain pathways over and over and over again, they become hardwired in the cortex  Activating one aspect will basically activate every single memory you ever had  Memories stronger: repeated activation or large emotional salient  Doesn’t work  Non-Declarative Memory/procedural memory: hippocampal independent  Skill memory: one type of non-declarative memory  Forms of skill human memory  Mirror tracing task: tracing a figure in a mirror  Mirror reading: ability to read in a mirror  Animal skill memory  Rotarod: Put rodents on a rotating rod and increase speed and they can get really good at this task and bet how long it takes for them to fall off  Acrobatic training: take rats and put them through a boot camp with obstacle courses, rope ladders, climb over objects, paw eye coordination  Visual water maze: becomes hippocampal independent task when platform is visible  Motor Cortex: where these memories are stored  Primary Motor cortex: Encode force and direction  Supplementary Motor Area: planning movements  Premotor cortex: planning and control limb movements  Cerebellum: motor skill that deals with balance will be stored in cerebellum  Priming: when an earlier stimulus influences the response to a later stimulus  Prefrontal cortex activated  Conditioning: when one stimuli predicts the delivery of a second stimuli


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