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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

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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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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...

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.
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If over time, all...

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Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...

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Related Experiment Video

Updated: Jul 12, 2026

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

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Published on: June 26, 2013

Ethanol effects on dentate granule cell LTP.

M J Wayner¹, D L Armstrong, C F Phelix

¹Department of Biology, University of Texas at San Antonio, 6900 N. Loop 1604 West, San Antonio, TX 78249, USA. mwayner@utsa.edu

Neurotoxicity Research

|April 28, 2004

Summary

Ethanol affects brain function, specifically the lateral hypothalamic area (LHA) and dentate gyrus. This study found higher ethanol concentrations are needed to impact the dentate gyrus directly compared to the LHA.

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Published on: June 26, 2013

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Published on: September 20, 2024

Area of Science:

Neuroscience
Neuropharmacology
Synaptic Plasticity

Background:

Previous studies identified a lateral hypothalamic area (LHA) sensitive to low ethanol concentrations (< 5.0 mM).
Angiotensin (Ang) in the LHA influences medial perforant path-dentate granule cell synapses via AT1 receptors, affecting long-term potentiation (LTP).
Losartan, an AT1 antagonist, prevents ethanol-induced impairment of LTP and behavior, implicating AT1 receptors.

Purpose of the Study:

To determine the dose-dependent effect of ethanol directly on LTP in the dentate gyrus.
To differentiate between direct effects of ethanol on the dentate gyrus versus indirect effects mediated by the LHA.

Main Methods:

Ethanol was directly perfused into the dentate gyrus of urethane-anesthetized rats using a cannula near the recording electrode.
Long-term potentiation (LTP) in medial perforant path-dentate granule cell synapses was measured.
Different concentrations of ethanol were administered to assess dose-dependent effects.

Main Results:

The threshold for ethanol to affect LTP in the dentate gyrus was significantly higher (> 30 mM and < 50 mM) than in the LHA.
Higher ethanol doses may exert direct effects on the LHA.
Elevated blood ethanol levels at higher doses could contribute to toxicity.

Conclusions:

Ethanol's impact on LTP in the dentate gyrus requires higher concentrations than its effect on the LHA.
Direct perfusion into the dentate gyrus helps distinguish local ethanol effects from systemic or LHA-mediated actions.
Ethanol may have dual effects: direct on the dentate gyrus at high concentrations and indirect via the LHA at lower concentrations.