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Related Concept Videos

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.
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 Potentiation01:35

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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.
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
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Caroline Kopp1, Fabio Longordo, Anita Lüthi

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular and Cellular Biology

Background:

  • N-methyl-D-aspartate receptors (NMDARs) are crucial for synaptic plasticity induction.
  • Synaptic activity modifies NMDAR composition and function, impacting future plasticity.
  • Homeostatic control of plasticity is established in developing sensory cortices.

Purpose of the Study:

  • To investigate whether NMDAR properties are altered in mature synapses.
  • To explore the role of behavioral manipulation and neurochemical signaling in NMDAR dynamics.
  • To understand how NMDAR function in mature synapses influences cognitive abilities.

Main Methods:

  • Analysis of NMDAR composition (e.g., NR2A/NR2B ratio) following behavioral manipulations.
  • Investigation of NMDAR trafficking regulation by G-protein-coupled receptors (e.g., orexin, dopamine).
  • Focus on mature glutamatergic synapses and their response to recent activity.

Main Results:

  • Behavioral manipulations (sensory experience, learning, sleep deprivation) alter the NR2A/NR2B ratio in hippocampal and cortical NMDARs.
  • NMDAR trafficking is modulated by neurotransmitter receptors involved in learning and arousal.
  • Mature glutamatergic synapses exhibit activity-dependent modifications in NMDAR function.

Conclusions:

  • Mature synapses dynamically adjust NMDAR function in response to recent activity.
  • NMDAR trafficking, influenced by neurochemical states, is a key mechanism for synaptic plasticity regulation.
  • These rapid NMDAR modifications may play a significant role in modulating adult cognitive functions.