Synaptic plasticity

Synaptic plasticity is the ability of connections between neurons to change in strength or structure. It supports learning, memory, and adaptation in neural circuits.

Long-term potentiation: A persistent increase in synaptic strength following particular patterns of neural activity. It is a major experimentally studied form of lasting synaptic strengthening.
Chemical synapse: A junction where one neuron communicates with another cell by releasing chemical neurotransmitters. Plasticity changes the transmission properties of this common form of neural junction.
Memory consolidation: The processes that stabilize newly formed memories over time. Persistent synaptic changes are candidate mechanisms for stabilizing stored memories.
Short-term synaptic plasticity: Transient changes in synaptic strength lasting milliseconds to minutes, often caused by recent activity. It contrasts with persistent changes that can last hours, days, or longer.
Long-term depression: A persistent decrease in synaptic strength following particular patterns of neural activity. It shows how synapses can weaken as well as strengthen.
Neurotransmitter: A chemical messenger released by neurons to signal across synapses or to other target cells. Release and reception of these messengers are frequent sites of synaptic modification.
Memory engram: A physical trace in neural tissue associated with the storage and later retrieval of a memory. Engram formation and recall involve changes in selected neural connections.
Homeostatic plasticity: Activity-dependent adjustments that stabilize a neuron's overall excitability or network activity. It regulates broad activity levels, unlike Hebbian changes tied to specific inputs.
Hebbian theory: A theory that connections strengthen when the neurons they link are repeatedly active together. It captures the activity-dependent rule underlying several forms of synaptic change.
Glutamate: The principal excitatory neurotransmitter in the mammalian central nervous system. Many studied forms of excitatory plasticity depend on glutamate signaling.

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