LTP and LTD

Malenka, R. C., & Bear, M. F. (2004). LTP and LTD: An Embarrassment of Riches. Neuron, 44(1), 5-21.

Type

Journal article

Intellectual base

Primary research

Year

2004

Volume

44

Issue

1

Pages

5-21

DOI

10.1016/j.neuron.2004.09.012

DOI registrant

Elsevier

Link

https://doi.org/10.1016/j.neuron.2004.09.012

Cited from

pharmacology_toxicology

Cited by

3 citations across 3 artifacts.

Each citation links to the sentence it supports in the citing article.

Primes

• Potentiation
  • The response shift reflects internal sensitization of the responding substrate—receptor up-regulation increasing the number of available binding sites, synaptic strengthening through insertion of additional receptors (AMPA insertion at potentiated synapses), signal-transduction amplification via kinase cascades and phosphorylation, or pathway priming in which a first stimulus prepares intracellular machinery for rapid amplified response to a second, mechanisms Malenka and Bear (2004) catalogue as the molecular foundation of LTP.

Domain-specific

• Neuroplasticity
  • The mechanism is activity-dependent modification of synaptic weights via long-term potentiation (LTP) and long-term depression (LTD), each mediated by NMDA-receptor coincidence detection and downstream calcium signalling cascades involving CaMKII, AMPA-receptor trafficking, and protein-synthesis-dependent consolidation for durable change

    This sourceReview of long-term potentiation and depression as the substrate of experience-dependent modification of brain function, which stresses that LTP and LTD are not unitary phenomena and that their mechanisms vary with the synapse and the circuit.

    Supported in partVerified against a saved copy of the source

    “LTP and LTD, the long-term potentiation and depression of excitatory synaptic transmission, are widespread phenomena expressed at possibly every excitatory synapse in the mammalian brain.”

    Read by an automated reader; not a human review. How support was checked

• Synaptic Plasticity
  • induced by high-frequency coincident pre- and postsynaptic activity and mediated by NMDA-receptor coincidence detection, calcium influx into the dendritic spine, CaMKII-dependent phosphorylation, trafficking of additional AMPA receptors to the postsynaptic density, and, for late-phase LTP, protein synthesis and structural spine growth; long-term depression (LTD) is the complementary synaptic weakening, induced by low-frequency or temporally asynchronous activity and mediated by phosphatase activation and AMPA-receptor internalisation

    This sourceThe Malenka and Bear Neuron review of LTP and LTD as widespread, non-unitary forms of long-term potentiation and depression of excitatory synaptic transmission whose mechanisms vary by synapse and circuit.

    Supported in partVerified against a saved copy of the source

    “LTP and LTD, the long-term potentiation and depression of excitatory synaptic transmission, are widespread phenomena expressed at possibly every excitatory synapse in the mammalian brain.”

    Read by an automated reader; not a human review. How support was checked

Verification

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Registry ID ref:e5f011cf821e · see in the full table