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Related Concept Videos

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.
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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.
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 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...
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

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.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...

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Related Experiment Video

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Combining Optogenetics with Artificial microRNAs to Characterize the Effects of Gene Knockdown on Presynaptic Function within Intact Neuronal Circuits
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Targeting calpain in synaptic plasticity.

Michel Baudry1, Maggie M Chou, Xiaoning Bi

  • 1Western University of Health Sciences, Graduate College of Biomedical Sciences, Basic Medical Sciences, COMP , 309 E 2nd St, Pomona, CA 91766, USA. mbaudry@westernu.edu

Expert Opinion on Therapeutic Targets
|February 6, 2013
PubMed
Summary
This summary is machine-generated.

Calpains, calcium-dependent proteases, are involved in cell functions and neurodegeneration. Inhibiting calpain activity may offer therapeutic benefits for conditions linked to synaptic plasticity deregulation.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Calpains are calcium-dependent proteases crucial for various cellular functions, including cell division, migration, and death.
  • In the central nervous system (CNS), µ-calpain and m-calpain isoforms are linked to synaptic plasticity and neurodegeneration.
  • This review focuses on the role of calpains in synaptic plasticity and their therapeutic potential.

Purpose of the Study:

  • To review the literature on calpain involvement in synaptic plasticity.
  • To explore the connection between calpain activity and learning impairments.
  • To discuss the potential for developing calpain-targeting therapeutics.

Main Methods:

  • Literature review of studies on calpains and synaptic plasticity.
  • Analysis of research linking calpains to learning and memory deficits.
  • Evaluation of therapeutic strategies targeting calpain activity.

Main Results:

  • Calpain activation is implicated in neurodegenerative processes and cancer.
  • A peptide targeting calpain demonstrated neuroprotective effects in neonatal hypoxia/ischemia models.
  • Calpain dysregulation is associated with altered synaptic plasticity.

Conclusions:

  • Therapeutic strategies involving calpain inhibition are of significant interest.
  • Development of selective calpain inhibitors or substrate-targeting drugs is needed.
  • Targeting calpains offers potential for treating conditions related to synaptic plasticity deregulation.