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Related Concept Videos

Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

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...
Adrenergic Agonists: Indirect-Acting Agents01:25

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...
Adrenergic Neurons: Neurotransmission01:27

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.
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...
Adrenergic Receptors: ɑ Subtype01:31

Adrenergic Receptors: ɑ Subtype

Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
CNS Stimulants: Cocaine, Amphetamines and Cannabinoids01:24

CNS Stimulants: Cocaine, Amphetamines and Cannabinoids

CNS stimulants, such as cocaine, amphetamines, and cannabinoids, have varying structures and mechanisms of action that lead to different therapeutic effects and side effects. Cocaine, with its molecular formula C17H21NO4, is a tropane alkaloid and a tertiary amino compound. It has two chemical forms: the hydrochloride salt and the "freebase." The former is in powder form, while the latter involves removing the hydrochloride salt to create a form that can be smoked. Cocaine exerts its effects by...

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Related Experiment Video

Updated: Jun 15, 2026

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
11:29

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Published on: September 4, 2015

Caffeine, adenosine receptors, and synaptic plasticity.

Ana Rita Costenla1, Rodrigo A Cunha, Alexandre de Mendonça

  • 1Institute of Pharmacology and Neurosciences, Faculty of Medicine and Unit of Neuroscience, Institute of Molecular Medicine, University of Lisbon, Lisbon, Portugal.

Journal of Alzheimer'S Disease : JAD
|February 26, 2010
PubMed
Summary
This summary is machine-generated.

Caffeine consumption in rats at concentrations relevant to humans attenuates hippocampal long-term potentiation (LTP), a key form of synaptic plasticity. These findings suggest caffeine

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Last Updated: Jun 15, 2026

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Published on: September 4, 2015

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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Limited research exists on caffeine's effects on synaptic plasticity at physiologically relevant concentrations.
  • Caffeine's primary action at low micromolar concentrations is adenosine receptor antagonism.

Purpose of the Study:

  • To investigate the impact of caffeine on hippocampal synaptic plasticity at concentrations mimicking human coffee consumption.
  • To explore the role of adenosine receptors in caffeine's effects on long-term potentiation (LTP).

Main Methods:

  • Rats consumed caffeine (1 g/L) for 3 weeks, achieving hippocampal concentrations of approximately 22 microM.
  • Electrophysiological recordings were performed on hippocampal slices to assess frequency-induced LTP.
  • The effects of low micromolar caffeine (30 microM) were examined in both young and aged animals.

Main Results:

  • Caffeine (30 microM) attenuated frequency-induced LTP in hippocampal slices, similar to selective adenosine A2A receptor antagonists.
  • These caffeine-induced effects on LTP were observed in aged animals, suggesting potential relevance for age-related cognitive function.

Conclusions:

  • Caffeine, at concentrations achieved through regular coffee intake, can modulate hippocampal synaptic plasticity.
  • The findings support a role for adenosine A2A receptors in mediating caffeine's effects on LTP.
  • Further research using pharmacological and genetic methods is needed to fully elucidate the involvement of adenosine A1 and A2A receptors.