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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.

Neuroplasticity

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.

Neurochemical Transmission: Sites of Drug Action

Neurochemical Transmission: Sites of Drug Action

Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...

Drugs Acting on Autonomic Ganglia: Stimulants

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Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...

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 13, 2026

Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine

Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine

Published on: January 25, 2019

Nicotine and synaptic plasticity in prefrontal cortex.

Daniel S McGehee¹

¹Department of Anesthesia and Critical Care, Committee on Neurobiology, University of Chicago, Chicago, IL 60637, USA. dmcgehee@uchicago.edu

Science'S STKE : Signal Transduction Knowledge Environment

|August 19, 2007

Summary

Nicotine enhances working memory by modulating brain signals in the prefrontal cortex. This effect involves altering inhibitory inputs to neurons, potentially improving treatments for memory disorders.

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Last Updated: Jul 13, 2026

Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine

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Published on: January 25, 2019

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Published on: November 29, 2013

Area of Science:

Neuroscience
Cognitive Science
Pharmacology

Background:

Working memory and attention are cognitive functions modulated by nicotinic acetylcholine receptors.
The prefrontal cortex is crucial for working memory, with synaptic plasticity being a key cellular mechanism.
Understanding nicotine's cellular effects in the prefrontal cortex is vital for cognitive enhancement research.

Purpose of the Study:

To investigate the cellular and synaptic mechanisms underlying nicotine's effects on prefrontal cortex excitability.
To explore how nicotinic receptor activation influences synaptic plasticity, specifically long-term potentiation (LTP).
To determine the impact of nicotine on neuronal signal processing relevant to working memory.

Main Methods:

Electrophysiological recordings in the prefrontal cortex.
Nicotinic receptor activation and stimulation of layer V pyramidal cells.
Assessment of long-term potentiation (LTP) induction and synaptic input modulation.

Main Results:

Nicotine enhances inhibitory synaptic inputs to layer V pyramidal cells.
This enhancement of inhibition suppresses the induction of LTP.
Burst stimulation of pyramidal cells can overcome nicotine-induced LTP suppression, altering the signal-to-noise ratio.

Conclusions:

Nicotinic receptor activity modulates synaptic plasticity in the prefrontal cortex through inhibitory pathways.
The findings suggest that nicotine can enhance the impact of strong stimuli on working memory.
This research may inform the development of novel therapeutic strategies for memory impairments.