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Related Concept Videos

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...
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.
Postsynaptic Potential (PSP)01:32

Postsynaptic Potential (PSP)

Postsynaptic potential (PSP) refers to a change in the electrical potential of a neuron when neurotransmitters released by presynaptic neurons bind to postsynaptic receptors. This potential can either be excitatory, leading to depolarization and ultimately action potential generation, or inhibitory, leading to hyperpolarization and suppression of the postsynaptic neuron.
There are two types of receptors: ionotropic and metabotropic.
The ionotropic receptor is the membrane protein that has an...
The Neuromuscular Junction01:19

The Neuromuscular Junction

The nervous system consists of complex motor neuron circuits, including upper motor neurons originating from the cerebral cortex and lower motor neurons starting in the spinal cord, coordinating both voluntary and involuntary movements. Among these, somatic motor neurons activate skeletal muscles and are classified into alpha, beta, and gamma types. Alpha neurons are vital for voluntary movement coordination, while gamma neurons adjust muscle spindle sensitivity, and the function of beta...
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific...
Action Potential01:14

Action Potential

Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
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Related Experiment Video

Updated: May 28, 2026

Simultaneous Pre- and Post-synaptic Electrophysiological Recording from Xenopus Nerve-muscle Co-cultures
08:13

Simultaneous Pre- and Post-synaptic Electrophysiological Recording from Xenopus Nerve-muscle Co-cultures

Published on: March 11, 2013

Postsynaptic TRPC1 function contributes to BDNF-induced synaptic potentiation at the developing neuromuscular

Julie S McGurk1, Sangwoo Shim, Ju Young Kim

  • 1The Solomon H. Snyder Department of Neuroscience, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|October 14, 2011
PubMed
Summary
This summary is machine-generated.

Brain-derived neurotrophic factor (BDNF) enhances synaptic strength by regulating calcium (Ca2+) dynamics. This study reveals Xenopus TRPC1 channels in postsynaptic cells are crucial for BDNF-induced potentiation at the neuromuscular junction.

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An Improved Protocol to Purify and Directly Mono-Biotinylate Recombinant BDNF in a Tube for Cellular Trafficking Studies in Neurons
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Levator Auris Longus Preparation for Examination of Mammalian Neuromuscular Transmission Under Voltage Clamp Conditions
10:45

Levator Auris Longus Preparation for Examination of Mammalian Neuromuscular Transmission Under Voltage Clamp Conditions

Published on: May 5, 2018

Related Experiment Videos

Last Updated: May 28, 2026

Simultaneous Pre- and Post-synaptic Electrophysiological Recording from Xenopus Nerve-muscle Co-cultures
08:13

Simultaneous Pre- and Post-synaptic Electrophysiological Recording from Xenopus Nerve-muscle Co-cultures

Published on: March 11, 2013

An Improved Protocol to Purify and Directly Mono-Biotinylate Recombinant BDNF in a Tube for Cellular Trafficking Studies in Neurons
13:46

An Improved Protocol to Purify and Directly Mono-Biotinylate Recombinant BDNF in a Tube for Cellular Trafficking Studies in Neurons

Published on: July 11, 2020

Levator Auris Longus Preparation for Examination of Mammalian Neuromuscular Transmission Under Voltage Clamp Conditions
10:45

Levator Auris Longus Preparation for Examination of Mammalian Neuromuscular Transmission Under Voltage Clamp Conditions

Published on: May 5, 2018

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular Biology

Background:

  • Brain-derived neurotrophic factor (BDNF) is known to potentiate synapses in the central nervous system (CNS) and neuromuscular junctions (NMJs).
  • The precise molecular mechanisms, particularly calcium (Ca2+) signaling pathways, underlying BDNF-induced synaptic plasticity remain incompletely understood.
  • Existing knowledge emphasizes presynaptic roles of Ca2+ in neurotrophin signaling.

Purpose of the Study:

  • To elucidate the molecular mechanisms of BDNF-induced synaptic potentiation at the Xenopus NMJ.
  • To investigate the role of calcium (Ca2+) dynamics and specific ion channels in BDNF signaling.
  • To identify the postsynaptic contribution to neurotrophin-mediated synaptic plasticity.

Main Methods:

  • Utilized the Xenopus NMJ in culture as a model system.
  • Employed pharmacological inhibition and morpholino-mediated knockdown of Xenopus TRPC1 (XTRPC1).
  • Assessed BDNF-induced changes in spontaneous synaptic response frequency, postsynaptic Ca2+ elevation, and receptor involvement (p75, TrkB).

Main Results:

  • Inhibition or knockdown of XTRPC1 significantly attenuated BDNF-induced potentiation of synaptic response frequency at the NMJ.
  • XTRPC1 was specifically required in postsynaptic myocytes for BDNF-induced Ca2+ elevation and full synaptic potentiation.
  • Blockade of the p75 neurotrophin receptor abolished BDNF-induced postsynaptic Ca2+ elevation and potentiating effects, while TrkB knockdown in postsynaptic myocytes had no impact.

Conclusions:

  • BDNF-induced synaptic potentiation involves coordinated presynaptic and postsynaptic mechanisms.
  • Xenopus TRPC1 channels play a critical postsynaptic role in mediating Ca2+ influx required for BDNF-induced synaptic plasticity.
  • This highlights a significant postsynaptic function of Ca2+ signaling in neurotrophin-induced synaptic plasticity, complementing its known presynaptic roles.