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Related Concept Videos

Long-term Potentiation01:35

Long-term Potentiation

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.
Long-term Potentiation01:25

Long-term Potentiation

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 presynaptic neurons...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...
Long-term Depression01:05

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
The Role of Ion Channels in Neuronal Computation01:19

The Role of Ion Channels in Neuronal Computation

A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.

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Modular competition driven by NMDA receptor subtypes in spike-timing-dependent plasticity.

Richard C Gerkin1, Pak-Ming Lau, David W Nauen

  • 1Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA.

Journal of Neurophysiology
|February 3, 2007
PubMed
Summary

Different N-methyl-d-aspartate receptor (NMDAR) subtypes mediate opposing roles in synaptic plasticity. NR2A-NMDARs facilitate potentiation, while NR2B-NMDARs drive depression, revealing a dynamic competition in neuronal signaling.

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular Biology

Background:

  • N-methyl-d-aspartate receptors (NMDARs) are crucial for synaptic plasticity.
  • The specific roles of different NMDAR subtypes in mediating plasticity remain debated.
  • Understanding NMDAR function is key to deciphering neuronal activity transduction.

Purpose of the Study:

  • To investigate the distinct roles of NMDAR subtypes in spike-timing-dependent plasticity (STDP).
  • To determine whether NR2A- and NR2B-containing NMDARs mediate opposing signaling pathways.
  • To explore the dynamic interplay between NMDAR subtypes during STDP induction.

Main Methods:

  • Perforated patch-clamp recordings in synaptically connected hippocampal neurons.
  • Pharmacological manipulation using NMDAR subtype-specific antagonists.
  • Analysis of spike-timing-dependent potentiation and depression.
  • Computational modeling to recapitulate experimental findings.

Main Results:

  • Spike-timing-dependent potentiation requires fast NMDAR currents mediated by NR2A-NMDARs.
  • Spike-timing-dependent depression involves slow NMDAR currents carried by NR2B-NMDARs.
  • Differential blockade of NMDAR subtypes alters the net outcome of STDP, indicating a competitive interaction.

Conclusions:

  • NR2A- and NR2B-containing NMDARs exhibit opposing roles in synaptic plasticity.
  • A dynamic competition between NMDAR subtypes regulates STDP.
  • Targeting specific NMDAR subtypes can bias plasticity outcomes, offering potential therapeutic avenues.