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learning / memory study guide

Difference Between Habituation and Sensitization:

  • Habituation: a decrease in response to a repeated, non-threatening, or irrelevant stimulus. 

    • The organism learns to ignore the stimulus because it is not significant. 

    • Reduces attention to unimportant stimuli.

  • Sensitization: An increase in response to a stimulus, often due to it being intense, harmful, or arousing.

    • The organism becomes more alert or reactive after exposure to a strong or noxious stimulus.

    • Enhances response to potential threats.

Kandel’s Three Hypotheses:

  1. Sensory neurons become less responsive.

    • The sensory neurons stop firing as strongly after repeated stimulation. 

  2. Motor neurons become fatigued.

    • The motor neurons that control the gill reflex eventually get tired and stop responding.

  3. Changes occur between the sensory and motor neurons. 

    • The weakening of the synapse between sensory and motor neurons. 

Which Hypothesis Is Correct?:

  • Changes are occurring between the sensory and motor neurons. 

  • Normally, sensory neurons depolarize as an influx of calcium enters the presynaptic terminal, triggering the release of glutamate into the synapse.

  • After repeated stimulation, fewer calcium channels open due to inactivation. 

    • Therefore, less calcium is released in the sensory neuron, causing less glutamate release into the synapse. 

  • With less glutamate, ESPSs become smaller and weaker.

    • Therefore, motor neurons will fire less strongly. 

Neural Mechanism for Habituation/Sensitization in Aplysia:

  • Aplysia is a good animal to study because it has fewer, but larger, neurons. 

  • The gill-withdrawal reflex explains:

    • The Aplysia’s gill is used for breathing and is covered with a mantle shelf, a protective tissue. 

    • Waste and seawater are released through the siphon, a tube-like structure.

    • Touching the siphon causes the gill to retract. 

  • Touching the siphon repeatedly leads to a less pronounced reflex or retraction of the gill. 

  • After an electrical shock to the head or tail, an Aplysia will show an increased gill-withdrawal response.

    • Sensory neurons release more neurotransmitters onto the interneurons and motor neurons, leading to a more intense response. 

What Are The Long-Term Changes?:

  • Typically, Aplysias show 1300 axon terminals synapsed with sensory neurons.

    • However, Aplysias that have experienced sensitization had 2800 terminals.

    • Aplysias that have experienced habituation have 800 terminals. 

Long-Term Potentiation:

  • The long-lasting increase in synaptic strength.

  • Thought to be associated with memory formation. 

  • LTP makes signal transmission faster and stronger.

  • NMDA and AMPA are receptors for glutamate.

  • Typically, only NMDA receptors are available to depolarize the postsynaptic membrane.

    • When the connection is strengthened, AMPA receptors are added to the membrane.

    • More AMPA receptors allow for a larger response to glutamate.

    • More AMPA receptors make it easier to reach depolarization (reaching threshold faster). 

    • This is the cellular basis for LTP.

Long-Term Depression:

  • The long-lasting decrease in synaptic strength that lasts hours or days.

  • Thought to be associated with learning. 

Evidence For LTP As A Mechanism For Long-Term Memory:

  • Both LTP and memories can last indefinitely.

  • Both LTP and memories can result from very brief input or events.

  • LTP is consistent with models proposed by Donald Hebb.

  • LTP is found in cells thought to be associated with memory formation, such as those in the hippocampus and cerebellum.

  • NMDA receptors (linked to LTP) are also linked to memory.

Amnesias:

  • Retrograde amnesia: loss of memories from the past.

  • Anterograde amnesia: inability to form new memories.

Patient H.M.:

  • Large areas of H.M.’s hippocampi and temporal lobes were surgically removed. 

  • His personality and IQ were not impacted.

  • However, he experienced profound retrograde amnesia as well as anterograde amnesia.

  • His short-term memory was ok.

    • “Working memory”

    • Could hold information for a very short amount of time when undistracted.

  • He could still learn procedural tasks.

    • Mirror drawing. He improved with practice despite not remembering ever doing it before. 

  • His deficits were in explicit memory tasks.

  • Concluded that the ability to store memories and the ability to access previously stored memories are in different brain areas.

  • Procedural memories are dealt with in different brain areas than explicit memories. 

Thalamus:

  • Korsakoff’s Syndrome:

    • Damage to the thalamus and the mammillary bodies

    • Caused by a thiamine deficiency due to alcoholism. 

  • Patient N.A.

    • A fencing foil went up his nose and caused a lesion to their left thalamus.

    • He had similar amnesia to H.M.

  • Delayed Non-Matching to Sample Task:

    • Monkeys with temporal lobe or thalamus damage could not do the DNMS task.

    • Requires the ability to transfer memories from short-term systems into long-term systems. 

Hippocampus:

  • The right hippocampus is active during spatial memory processing.

    • May include a 3D representation of the world around us.

  • The left hippocampus is more active during verbal memory tasks.

Prefrontal Cortex:

  • Patients with prefrontal cortex damage have issues with the Wisconsin card-sorting task.

    • Short-term memory issues.

  • Object permanence studies:

    • Adult monkeys with prefrontal damage don’t seem to grasp object permanence.

    • Prefrontal cortex is constantly developing throughout youth and childhood.

    • Object permanence usually develops in the first year of life. 

Basal Ganglia:

  • Lesions of the basal ganglia impact procedural memories, but not explicit memories.

    • The opposite of H.M.

  • Diseases that lead to damage to the basal ganglia typically also have procedural memory deficits.

    • Huntington’s and Parkinson’s Disease

Cerebellum:

  • Possibly key to procedural memories.

    • Motor learning

  • It is unclear and not currently agreed upon whether damage to the cerebellum leads to deficits in motor learning or simply the performance of that learned task.

Papez’s Circuit:

  • A network that connects the thalamus, mammillary bodies, and hippocampus.

    • Believed to be key to forming long memories. 

Stress and Memory:

  • Stress impacts the amygdala.

    • Has connections to the hippocampus.

  • Cortisol may damage the hippocampus.

    • Repression

    • Flashbacks/flashbulb memories