4. Learning & Memory

4. Learning & Memory

1. Amnesia

   • HM = had his medial temporal lobe removed to treat his seizures. It worked, but it also caused severe anterograde amnesia. Retrograde amnesia was graded, poor just before surgery and better as memories got older (temporal gradient)
   • Anterograde amnesia = damage temporal lobe leads to deficit in learning new memories or remembering anything after damage
   • Retrograde amnesia = deficit in remembering information before the damage
   • Declarative memory = Squire suggested procedural and declarative memory functions. Declarative split into episodic and semantic memory functions (Tulving)
   • Spared abilities in Amnesia: working memory, STM for implicit abilities, e.g. procedural and perceptual and stimulus-response

2. Models

   • Dual Process Hypothesis
     • Brown & Aggleton (2001) = Hippocampus and PRC contribute separately to memory, but are interacting
     • Hippocampus = prior occurence of information, including episodic information (Episodic)
     • PRC = discriminates familiarity and recency of stimuli (place/time)
     • Papez circuit (1937) = suggests many structures including the hippocampus, cingulate gyrus, anterior thalamic nuclei and mammilary bodies function in cortical control of emotion and memory storage
   • Single Process Hypothesis
     • Suggests knowing (familiarity) is a weaker trace of remembering (recollection)
     • Not 2 separate systems for familiarity and recollection
   • Animal
     • Michkin (1978) primates conducted a non-matching task, in different conditions. Those with large lesions like HM performed the worst. Those with hippocampal and temporal lesions performed around 50% and those with only hippocampal lesions performed slightly impaired. Suggests hippocampus is not involved in decalrative memory
     • Nemanic et al (2004) another study with monkeys, finding those with hippocampal lesions memory was fine but those with PRC lesions memory was severly impaired
   • Hippocampus = episodic and recollection. Perirhinal cortex = object memory, familiarity, and declarative memory

3. Neural Mechanisms

   • Neurons receive information from external environment, relay information to sensory neurons and send commands to motor muscles to respond appropriately
   • Kandel
     • Habituation =changes in neural activity related to hippocampal functioning
     • Stimulated an aplysia = touch its gill and it withdraws itself, but after a while it stops withdrawing (habituates)
     • Homosynaptic depression = habituation only occurs in the organ being stimulated
     • Short term = reduction of neurotransmitter released changes withdrawal response
     • Long term = change in circuit = reduction of number of synaptic connection between sensory and motor neurons
   • Action potential = reaches pre-synaptic terminal > calcium flows into axon > vesicles bind to receptors > neurotransmitter released > ions flow in = threshold reached = action potential
   • Hebb (1949)
     • synaptic plasticity rises memory function
     • cells that fire together, fire together
     • changes in memory and neuron functioning = learning

4. Place Cells

   • O'Keefe & Dostrovsky (1971)
     • considered activity of pyramidal cells in the hippocampus of rats
     • found a clump of cells fire at a higher rate when in certain locations = place cells
     • controlled by external environemntal cues
     • place cells combined form a cognitive map of environments
     • Wood et al (2000) suggested place cells provide information more than place within environment, also suggest the direction an animal is going to take next in a maze
   • Best, White & Manai (2001) suggested place cells are in dorsal hippocampus in rats and in posterior hippocampus in humans
   • Derikman & Moser (2010)
     • found other cells within the entorhinal cortex
     • Grid cells = coverage of the whole environment, forming a grid of the map of environment. Work together with place cells
     • Border cells = fire when near boundaries of the environment
     • Head direction cells = fire when the animal is facing a particualr direction
     • maps of event memory

5. LTP

   • Electrical stimulation of circuits within the hippocampus
   • LTP leads to changes of neural activity and learning occurs, but there is a short window for this to occur
   • Only occurs if the release of glutamate coincides with the depolarisation of neuron C
   • Bliis (2018) showed that NMDA receptors are dependent for LTP which represents synaptic memory learning
   • Plasticity = strengthening of synapses occurs by AMPA insertion into axon

6. Blocking NMDA

   • Optogenetics = new technology for manipulating AMPA and NMDA receptors to find support for Hebb's ideas
   • AP5
     • drug block NMDA, preventing calcium ions and prevents LTP
     • only block NMDA = selective antagnoist
     • if NDMA and is involved in learning = blocking NMDA prevents the formation of memories
   • Morris (1982) studies administering AP5
     • hippocampal lesioned rats dont learn to find the platform, but they do learn to swim around the pool at a fixed distance until they find the platform eventually
     • Ap5 group acquire tasks slower and they can't remember tak, but not visual discrimination
     • AP5 blocks NDMA = involved memory retrieval

7. Pavlov Conditioning

   • AMPA receptors = mediate normal synaptic transmission, allows sodium to change the resting potential of an axon
   • Pavlov conditioned dogs to salivate (C) when they heard a bell (A) as it was continuously paired with food (B)
   • Memory representations of neurons
   • Condition A to cause cell C when paired with B
   • NMDA receptors = control calcium ion channels, normally blcoked my mg so needs a chnage in potential to push mg out
   • Neuron B fires > AP hits pre-synaptic terminal > glutamate is released > AMPA channels open and release sodium > interacts with mg in NMDA channel > glutamate binds to NMDA > calcium released from NMDA to neuron C causing AP

8. Hippocampus

   • H = episodic memory and recollection
   • Milner, Vrohin & Tueber (1968) = made conclusions from the case of HM = HM couldnt remember over long periods so not LTM, he also couldnt make new memories so not STM = H must be involved in converting memories from STM to LTM
   • Declarative memories
     • processes and modifies memories
     • Smith & Squire (2009) suggested memories are initially stored in the hippocampus but as they are consoliaded, they are transferred to tne neocortex
   • Spatial Memory
     • HM couldnt find way around his environment
     • Studies shows rats with hippocampal lesions are impaired at finding their way around the environment
     • Studies on London Taxi drivers = with very good spatial knowledge = have increased hippocampal regions
   • Neurogenesis
     • new neurons are formed in the brain
     • for relational tasks = new neruons doubled
     • · Frankland, Kohler & Josselyn (2013) suggest new neurons which change the pattern of hippocampal rates = make new memories but forget older ones
   • Memory Consolidation
     • studies suggest mice in watermaze then hippomcapus removed = no colsidation
   • Reconsolidation of memories
     • modfication of LTM
     • altered attachement of memories

9. History

   • Gall = suggested the cranium is related to cognitive function. He felt the bumps on peoples skulls and attributed them to personality traits
   • Broca = identified specific deficits from lesions to the frontal lobe = Broca's aphasia due to left frontal damage
   • Wernicke = identified language deficits related to the superior temporal lobe = Wernicke Aphasia due to left temporal lobe damage
   • Lashley = suggested specific cortex areas contribute to memory functions. Removed parts of rats cortex to test his suggestion, finding specific parts related to functions
   • Bechterew = suggested memory deficits associated with softening of the temporal lobes (including the hippocampus)