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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.

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 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 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...

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Related Experiment Video

Updated: Jul 10, 2026

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

2-Deoxyglucose-induced long-term potentiation of monosynaptic IPSPs in CA1 hippocampal neurons.

K Krnjević¹, Y T Zhao

¹Anaesthesia Research Department, McGill University, Montreal, Quebec H3G 1Y6, Canada.

Journal of Neurophysiology

|February 11, 2000

Summary

This summary is machine-generated.

2-deoxyglucose (2-DG) can induce long-term potentiation (LTP) in inhibitory synapses, similar to excitatory synapses. This potentiation, observed in hippocampal CA1 neurons, suggests a presynaptic mechanism and is most significant without glutamate antagonists.

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Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

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Related Experiment Videos

Last Updated: Jul 10, 2026

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

Longitudinal Two-Photon Imaging of Dorsal Hippocampal CA1 in Live Mice

Longitudinal Two-Photon Imaging of Dorsal Hippocampal CA1 in Live Mice

Published on: June 19, 2019

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

Published on: August 11, 2019

Area of Science:

Neuroscience
Synaptic Plasticity
Cellular Electrophysiology

Background:

Previous studies demonstrated 2-deoxyglucose (2-DG) induced long-term potentiation (LTP) in excitatory synapses in the CA1 region.
The effect of 2-DG on inhibitory synaptic transmission remained largely unexplored.

Purpose of the Study:

To investigate whether 2-DG can induce LTP in inhibitory synapses.
To determine the characteristics and potential mechanisms of 2-DG-induced LTP in inhibitory synapses.

Main Methods:

Recording of pharmacologically isolated monosynaptic inhibitory postsynaptic potentials (IPSPs) and currents (IPSCs) in CA1 neurons.
Application of 2-deoxyglucose (2-DG) with and without N-methyl-D-aspartate (NMDA) receptor antagonists.
Analysis of early and late components of IPSPs/IPSCs to assess potentiation.

Main Results:

Overall significant potentiation of IPSP conductance (early component: 35.1%, late component: 36.5%) was observed.
Potentiation was statistically significant primarily when 2-DG was applied without glutamate antagonists.
The consistent potentiation of both early and late IPSP components suggests a presynaptic mechanism.

Conclusions:

2-deoxyglucose (2-DG) induces long-term potentiation (LTP) in inhibitory synapses in the CA1 region, albeit with greater variability than in excitatory synapses.
The findings suggest a presynaptic locus for 2-DG-induced LTP.
The results indicate that 2-DG-induced LTP of inhibitory synapses shares similarities with that of excitatory synapses.