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Related Concept Videos

Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
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Adrenergic Neurons: Neurotransmission

Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
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Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
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Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
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The sympathetic division can influence tissues and organs by releasing norepinephrine at peripheral synapses and distributing epinephrine and norepinephrine through the bloodstream. In times of crisis or stress, sympathetic activation occurs, which is regulated by sympathetic centers in the hypothalamus. As a result, sympathetic activation prepares the body for physical exertion, rapid ATP production, and heightened alertness, allowing individuals to respond effectively to challenging or...
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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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Related Experiment Video

Updated: Jun 5, 2026

Vagus Nerve Stimulation as a Tool to Induce Plasticity in Pathways Relevant for Extinction Learning
11:02

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Published on: August 21, 2015

Deepened extinction following compound stimulus presentation: noradrenergic modulation.

Patricia H Janak1, Laura H Corbit

  • 1Ernest Gallo Clinic and Research Center, University of California at San Francisco, Emeryville, California 94608, USA.

Learning & Memory (Cold Spring Harbor, N.Y.)
|January 13, 2011
PubMed
Summary

Increasing noradrenergic activity during extinction learning enhances the extinction of appetitive stimulus-reward memories. This finding suggests potential therapeutic strategies for relapse prevention in addiction and anxiety disorders.

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Last Updated: Jun 5, 2026

Vagus Nerve Stimulation as a Tool to Induce Plasticity in Pathways Relevant for Extinction Learning
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Extinction Training During the Reconsolidation Window Prevents Recovery of Fear
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Extinction Training During the Reconsolidation Window Prevents Recovery of Fear

Published on: August 24, 2012

Area of Science:

  • Neuroscience
  • Behavioral Pharmacology
  • Learning and Memory

Background:

  • Behavioral extinction is a learning process where previously rewarded stimuli are no longer followed by reward.
  • Extinction learning is susceptible to disruption by factors like reward cues, time passage, and context changes.
  • Previous research indicates that compound stimuli during extinction enhance learning.

Purpose of the Study:

  • To investigate the pharmacological basis of enhanced extinction learning observed with compound stimuli.
  • To test the hypothesis that noradrenergic activity modulates extinction of appetitive memories.

Main Methods:

  • Rats were trained in a lever-press task for food reward, followed by extinction training.
  • Systemic administration of saline, yohimbine (α2 antagonist), atomoxetine (norepinephrine reuptake inhibitor), or propranolol (β-receptor antagonist) occurred before an extinction session.
  • Spontaneous recovery of responding was assessed four weeks later.

Main Results:

  • Increased noradrenergic activity during extinction training augmented extinction learning.
  • Animals treated to increase noradrenergic activity showed less spontaneous recovery of responding.
  • Blockade of noradrenergic activity did not impair extinction learning in this paradigm.

Conclusions:

  • Noradrenergic system activation during extinction enhances the consolidation of nonreward predictions.
  • These findings support the role of noradrenergic activity in reducing the return of extinguished responses.
  • Implications for developing therapies for relapse in addiction and other conditions involving disrupted extinction.