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Related Concept Videos

Long-term Potentiation01:35

Long-term Potentiation

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when...
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Calmodulin-dependent Signaling01:16

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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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Catenins01:23

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Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
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The adherens junctions that anchor cells together are multi-protein complexes that dynamically adapt to mechanical stimuli such as tensile forces and shear stress. Mechanosensory proteins in these junctions can sense such mechanical stimuli and undergo a shift in their conformation, resulting in an altered function — a process called mechanotransduction.
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Emotionally traumatic events often lead to memories that are exceptionally vivid and enduring, sometimes persisting with remarkable clarity throughout an individual's life. A classic example of this phenomenon is a person who survives a car accident. Even years later, they may recall every detail of the event with startling accuracy — the screeching of the tires, the jarring impact, and the acrid smell of burning rubber. Such vividness contrasts sharply with how an individual...
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Related Experiment Video

Updated: May 4, 2026

T-maze Forced Alternation and Left-right Discrimination Tasks for Assessing Working and Reference Memory in Mice
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Alpha-CaMKII-dependent plasticity in the cortex is required for permanent memory.

P W Frankland1, C O'Brien, M Ohno

  • 1Departments of Neurobiology, Psychiatry and Psychology, Brain Research Institute, University of California, Los Angeles, California 90095-1761, USA.

Nature
|May 18, 2001
PubMed
Summary

Alpha-calcium-calmodulin kinase II (alpha-CaMKII) is crucial for long-term memory consolidation in the cortex. Impaired alpha-CaMKII function in mice disrupts permanent memory traces, highlighting its role in synaptic plasticity.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cognitive Science

Background:

  • Cortical plasticity is essential for forming lasting memories.
  • The molecular mechanisms of memory consolidation in cortical networks are not well understood.

Purpose of the Study:

  • To investigate the role of alpha-calcium-calmodulin kinase II (alpha-CaMKII) in the consolidation of long-term memories in cortical networks.
  • To explore the molecular and cellular processes underlying permanent memory trace establishment.

Main Methods:

  • Utilized heterozygous alpha-calcium-calmodulin kinase II null mutant mice (alpha-CaMKII+/-).
  • Assessed learning and memory in hippocampus-dependent tasks at various retention delays (1-50 days).
  • Measured long-term potentiation (LTP) in cortical and hippocampal slices.

Main Results:

  • Alpha-CaMKII+/- mice exhibited normal learning and short-term memory (1-3 days).
  • Long-term memory (10-50 days) was significantly impaired in alpha-CaMKII+/- mice.
  • Cortical LTP was impaired in alpha-CaMKII+/- mice, while hippocampal LTP remained unaffected.

Conclusions:

  • Alpha-Ca-calmodulin kinase II plays a critical role in the consolidation of long-term memories within cortical networks.
  • Alpha-CaMKII appears to modulate synaptic events necessary for establishing permanent memory traces.
  • These findings provide insights into the molecular mechanisms of memory consolidation.