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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.

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Published on: March 23, 2011

A delayed response enhancement during hippocampal presynaptic plasticity in mice.

Vidar Jensen¹, S Ivar Walaas, Sabine Hilfiker

¹Molecular Neurobiology Research Group (MONERG), PO Box 1104, Faculty of Medicine, University of Oslo, N-0317 Blindern, Oslo, Norway.

The Journal of Physiology

|June 16, 2007

Summary

Researchers discovered a novel delayed enhancement in synaptic efficacy during prolonged stimulation of mouse hippocampal synapses. This effect, dependent on F-actin and synapsins, helps maintain synaptic function during sustained neural activity.

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Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

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Published on: January 1, 2018

Area of Science:

Neuroscience
Synaptic Plasticity

Background:

High-frequency stimulation typically causes short-term synaptic efficacy increases, followed by depression due to vesicle depletion.
Understanding mechanisms that maintain synaptic function during prolonged activity is crucial.

Purpose of the Study:

To identify and characterize a novel, delayed enhancement phase of synaptic response.
To investigate the molecular and cellular underpinnings of this delayed enhancement in hippocampal synapses.

Main Methods:

Electrophysiological recordings of excitatory glutamatergic synapses in adult mouse CA1 hippocampal slices.
Stimulation at frequencies of 5-20 Hz at physiological and reduced temperatures (24°C).
Assessment of F-actin and synapsin dependence, and exclusion of other contributing factors like presynaptic action potentials or inhibitory neurotransmission.

Main Results:

A delayed, transient response enhancement phase was observed during prolonged stimulation (5-20 Hz).
This enhancement was temperature-dependent, prominent at physiological temperatures, and absent at 24°C.
The effect required intact F-actin filaments and the presence of synapsins I and/or II.
The enhancement phase interrupted synaptic decay and lasted for approximately 75 stimuli at 5-10 Hz.

Conclusions:

A novel delayed enhancement mechanism contributes to synaptic efficacy maintenance during prolonged excitatory activity.
This mechanism involves F-actin and synapsins, suggesting a role in regulating a restricted pool of synaptic vesicles.
This finding offers new insights into the dynamic regulation of synaptic strength in the hippocampus.