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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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Allosteric regulation of enzymes occurs when the binding of an effector molecule to a site that is different from the active site causes a change in the enzymatic activity. This alternate site is called an allosteric site, and an enzyme can contain more than one of these sites. Allosteric regulation can either be positive or negative, resulting in an increase or decrease in enzyme activity. Most enzymes that display allosteric regulation are metabolic enzymes involved in the degradation or...
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Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
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Enhancing NMDA Receptor Function: Recent Progress on Allosteric Modulators.

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Researchers are developing new ways to boost N-methyl-D-aspartate receptor (NMDAR) function. These NMDAR positive modulators offer potential new treatments for brain diseases like Alzheimer's and schizophrenia.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • N-methyl-D-aspartate receptors (NMDARs) are crucial for brain function, involved in neurotransmission and synaptic plasticity.
  • Dysregulation of NMDARs (hypo- or hyperactivation) is implicated in neurological and psychiatric disorders such as stroke, schizophrenia, depression, and Alzheimer's disease.

Purpose of the Study:

  • To review recent advancements in enhancing NMDAR function, shifting focus from inhibition to potentiation.
  • To highlight the development and therapeutic potential of subunit-selective, allosteric positive modulators (PAMs) of NMDARs.

Main Methods:

  • Literature review focusing on recent research in NMDAR pharmacology.
  • Analysis of novel NMDAR positive allosteric modulators (PAMs) and their mechanisms.
  • Discussion of therapeutic strategies targeting NMDAR enhancement.

Main Results:

  • Significant progress has been made in designing subunit-selective NMDAR allosteric positive modulators.
  • These novel NMDAR-PAMs demonstrate potential for therapeutic applications by restoring NMDAR function.

Conclusions:

  • Enhancing NMDAR function, particularly through subunit-selective PAMs, represents a promising therapeutic avenue for brain diseases.
  • Further research into NMDAR-PAMs is warranted to explore their clinical utility in conditions associated with NMDAR hypofunction.