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Related Concept Videos

Long-term Potentiation

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 Potentiation

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 Depression

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 Depression

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...

Excitatory and Inhibitory Effects of Neurotransmitters

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...

Integration of Synaptic Events

Integration of Synaptic Events

Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...

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Related Experiment Video

Updated: Jun 23, 2026

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Published on: September 4, 2015

Synaptotagmin-IV modulates synaptic function and long-term potentiation by regulating BDNF release.

Camin Dean¹, Huisheng Liu, F Mark Dunning

¹Department of Physiology, University of Wisconsin, Madison, Wisconsin, USA.

Nature Neuroscience

|May 19, 2009

Summary

Synaptotagmin-IV (syt-IV) regulates brain-derived neurotrophic factor (BDNF) release from neurons, impacting synaptic plasticity and learning. This protein controls BDNF secretion, influencing synaptic strength and memory formation.

More Related Videos

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

Published on: June 26, 2013

Real-time Imaging of Axonal Transport of Quantum Dot-labeled BDNF in Primary Neurons

Real-time Imaging of Axonal Transport of Quantum Dot-labeled BDNF in Primary Neurons

Published on: September 15, 2014

Related Experiment Videos

Last Updated: Jun 23, 2026

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Published on: September 4, 2015

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

Published on: June 26, 2013

Real-time Imaging of Axonal Transport of Quantum Dot-labeled BDNF in Primary Neurons

Real-time Imaging of Axonal Transport of Quantum Dot-labeled BDNF in Primary Neurons

Published on: September 15, 2014

Area of Science:

Neuroscience
Molecular Biology
Cell Biology

Background:

Synaptotagmin-IV (syt-IV) is a protein involved in membrane trafficking.
Its precise localization and function in synaptic plasticity, learning, and memory are not fully understood.
Understanding syt-IV's role is crucial for deciphering synaptic function.

Purpose of the Study:

To investigate the localization and function of syt-IV in hippocampal neurons.
To elucidate the role of syt-IV in regulating brain-derived neurotrophic factor (BDNF) release.
To determine the impact of syt-IV on synaptic vesicle dynamics and long-term potentiation (LTP).

Main Methods:

Immunolocalization studies to identify syt-IV localization within neurons.
Analysis of BDNF-containing vesicle exocytosis in axons and dendrites.
Genetic manipulation (knockout and overexpression) of syt-IV.
Electrophysiological recordings to assess synaptic transmission and LTP.

Main Results:

Syt-IV was found to localize to BDNF-containing vesicles in hippocampal neurons.
Syt-IV inhibited BDNF release from both axonal and dendritic vesicles.
Loss of syt-IV enhanced synaptic vesicle exocytosis and LTP, mediated by BDNF release.
Selective loss of presynaptic syt-IV increased spontaneous quantal release, while postsynaptic loss increased quantal amplitude.

Conclusions:

Postsynaptic syt-IV regulates trans-synaptic BDNF action to control presynaptic vesicle dynamics.
Syt-IV acts as a key regulator of BDNF secretion, influencing synaptic strength.
The modulation of BDNF release by syt-IV is a critical mechanism for maintaining synaptic function during LTP.