Neuroscience of Memory and Synaptic Plasticity

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These vocabulary flashcards cover key scientists, theories, learning types, synaptic mechanisms, molecular players, and properties central to memory and synaptic plasticity as presented in the lecture notes.

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46 Terms

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Hermann Ebbinghaus

  • Forgetting curve – Memory fades over time.

  • Spacing effect – Spaced studying helps long-term memory.

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Forgetting curve

Graph showing how memory retention declines over time without reinforcement.

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Spacing effect

Improved long-term retention when learning sessions are spread out over time rather than massed together.

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Georg Müller

Researcher who discovered and introduced the concept of memory consolidation.

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Memory consolidation

Process by which short-term memories are stabilized into long-term storage.

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Camillo Golgi

An old idea that said all brain cells (neurons) are connected together in one big network without any gaps.

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Reticular theory

Discredited idea that nervous tissue is a single interconnected web without discrete cells.

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Santiago Ramón y Cajal

Neuroscientist who established the neuron doctrine and argued neurons are individual cells.

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Neuron doctrine

Principle that neurons are separate, discrete units communicating via specialized contacts (synapses).

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Terje Lømo

Norwegian scientist who discovered long-term potentiation (LTP) in 1973.

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Long-Term Potentiation (LTP)

Enduring increase in synaptic strength produced by high-frequency stimulation; model for learning and memory.

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Non-associative learning

Learning where your response gets stronger or weaker to one repeated thing — either by getting used to it (habituation) or becoming more sensitive to it (sensitization).

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Habituation

Progressive decrease in behavioral response to a repeated, harmless stimulus.

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Sensitization

Enhanced response to a stimulus following exposure to a strong or noxious event.

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Associative learning

Learning that links two stimuli or a stimulus and a response, as in classical conditioning.

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Classical conditioning

Learning by connecting two things — like a sound and food — so that one starts to cause the same reaction as the other

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Conditioned stimulus (CS)

Something that starts to cause a reaction after being paired with something important

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Unconditioned stimulus (US)

Something that naturally causes a reaction, without any learning.

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Conditioned response (CR)

Learned reaction produced by the conditioned stimulus after conditioning.

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Excitatory postsynaptic potential (EPSP)

Depolarizing change in membrane potential that makes a neuron more likely to fire an action potential.

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Inhibitory postsynaptic potential (IPSP)

Hyperpolarizing change in membrane potential that decreases the likelihood of neuronal firing.

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Action potential

All-or-none electrical impulse that rapidly travels along an axon to transmit neural information.

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Excitatory synapse

Synaptic connection that releases glutamate to generate EPSPs in the postsynaptic neuron.

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Inhibitory synapse

Synaptic connection that releases GABA to generate IPSPs in the postsynaptic neuron.

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Neurotransmitter life cycle

Sequence of synthesis, vesicular storage, release, receptor binding, and removal (reuptake or degradation) of a neurotransmitter.

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Long-Term Depression (LTD)

Persistent weakening of synaptic strength produced by low-frequency stimulation or weak Ca²⁺ signals.

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Tri-synaptic pathway

Hippocampal circuit: Entorhinal cortex → Dentate gyrus → CA3 → CA1.

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High-frequency stimulation

Rapid trains of impulses that raise intracellular Ca²⁺ levels and induce LTP.

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Low-frequency stimulation

Sparse impulses that cause modest Ca²⁺ entry and promote LTD.

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Kinase

Enzyme activated by high Ca²⁺ that phosphorylates proteins, facilitating LTP.

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Phosphatase

Enzyme activated by low Ca²⁺ that removes phosphates, contributing to LTD.

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Calcium model of plasticity

Theory that the magnitude of Ca²⁺ influx determines whether a synapse undergoes LTP (high Ca²⁺) or LTD (low Ca²⁺).

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AMPA receptor (AMPAR)

Ionotropic glutamate receptor; insertion into the postsynaptic membrane increases synaptic strength during LTP.

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NMDA receptor (NMDAR)

Voltage- and ligand-gated glutamate receptor that admits Ca²⁺ only when glutamate is present and the membrane is depolarized; acts as a coincidence detector.

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CaMKII

Calcium/calmodulin-dependent protein kinase II that is activated by Ca²⁺ and drives AMPAR insertion during LTP.

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Constitutive AMPAR pathway

Continuous, basal recycling of AMPA receptors to and from the synaptic membrane.

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Regulated AMPAR pathway

Activity-dependent trafficking of AMPARs, especially during LTP induction.

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AMPAR endocytosis

Removal of AMPA receptors from the postsynaptic membrane during LTD, weakening the synapse.

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Input specificity

Only synapses that receive stimulation undergo LTP; neighboring inactive synapses do not.

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Associativity (LTP property)

Weak synaptic input can be potentiated if it occurs simultaneously with strong input to the same postsynaptic cell.

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Cooperativity

Multiple weak inputs can collectively generate enough depolarization to induce LTP.

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Persistence

LTP can last from hours to the entire lifetime of an organism.

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Activity dependence

Induction of LTP requires coincident pre- and postsynaptic activity.

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Hebb’s Law

Principle stating that “neurons that fire together wire together,” underlying synaptic strengthening.

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Cajal’s memory hypothesis

Proposal that synapses are the primary sites where memories are stored.

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Jerzy Konorski

Neuroscientist who, in 1948, independently proposed the idea of synaptic plasticity as a basis for learning.