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Related Concept Videos

Long-term Depression01:03

Long-term Depression

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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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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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Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
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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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Chemical Synapses

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Related Experiment Video

Updated: Jan 5, 2026

Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis
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Calcium Dynamics and Synaptic Plasticity.

Pedro Mateos-Aparicio1, Antonio Rodríguez-Moreno2

  • 1Laboratorio de Neurociencia Celular y Plasticidad, Departamento de Fisiología, Anatomía y Biología Celular, Universidad Pablo de Olavide, Sevilla, Spain. pmatmor@upo.es.

Advances in Experimental Medicine and Biology
|October 25, 2019
PubMed
Summary
This summary is machine-generated.

Synaptic plasticity, crucial for learning and memory, involves calcium (Ca2+)-dependent processes. This chapter explores how Ca2+ drives various forms of synaptic plasticity in neurons.

Keywords:
AMPAKinasesLTDLTPNMDASecond messengersShort-term plasticitySynaptic plasticityTransmitter releasecalcium

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Area of Science:

  • Neuroscience
  • Cellular Biology

Background:

  • Synaptic plasticity refers to activity-dependent changes in synaptic strength.
  • These changes are vital for learning, memory, and brain development.
  • Calcium (Ca2+) ions play a critical role in synaptic plasticity.

Purpose of the Study:

  • To elucidate the Ca2+-dependent mechanisms underlying synaptic plasticity.
  • To detail the role of Ca2+ in the induction and expression of synaptic plasticity.

Main Methods:

  • Focus on Ca2+-mediated events.
  • Review of established literature on synaptic plasticity.

Main Results:

  • Ca2+ is indispensable for multiple forms of synaptic plasticity.
  • Specific Ca2+-dependent pathways are crucial for synaptic efficacy changes.

Conclusions:

  • Calcium signaling is a universal mechanism in synaptic plasticity.
  • Understanding these Ca2+-dependent events is key to comprehending brain function and disorders.