Related Experiment Video
Updated: May 9, 2026
15:27
Construction of Vapor Chambers Used to Expose Mice to Alcohol During the Equivalent of all Three Trimesters of Human Development
Published on: July 13, 2014
Adenosine receptor antagonists including caffeine alter fetal brain development in mice
Carla G Silva1, Christine Métin, Walid Fazeli
1Aix Marseille Université, INS, 13005 Marseille, France. c.gomesdasilva@gmail.com
Science Translational Medicine
|August 9, 2013
Summary
Prenatal exposure to adenosine type 2A receptor (A2AR) antagonists, including caffeine, can disrupt fetal brain development. This may lead to lasting neurological and cognitive issues in offspring.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Maternal substance consumption during pregnancy can negatively impact fetal brain development.
- Adenosine receptors play a crucial role in neural development.
Purpose of the Study:
- To investigate the effects of adenosine type 2A receptor (A2AR) antagonists on neural development in offspring.
- To determine if caffeine exposure during pregnancy affects offspring neurodevelopment.
Main Methods:
- Mouse dams were exposed to an A2AR antagonist or caffeine during pregnancy and lactation.
- Offspring neurodevelopment, including GABA neuron migration and hippocampal circuitry, was assessed.
- Neuronal network excitability and seizure susceptibility were evaluated.
Main Results:
- A2AR antagonist or caffeine exposure delayed GABA neuron migration and insertion into the hippocampus.
- Increased neuronal network excitability and seizure susceptibility were observed in offspring.
- Adult offspring showed loss of hippocampal GABA neurons and cognitive deficits.
Conclusions:
- Prenatal and lactational exposure to A2AR antagonists, including caffeine, adversely affects offspring neural development.
- These findings highlight potential risks associated with maternal caffeine consumption during pregnancy.
- Further research is needed to understand the long-term neurological consequences.
Related Concept Videos
01:29Drugs 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...
01:21Drugs 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...
01:07Teratogenicity
The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
01:29Stimulants
Stimulants are substances that enhance neural activity and elevate dopamine levels in the brain, leading to their highly addictive nature. These drugs include cocaine, amphetamines, MDMA, caffeine, and nicotine, each with distinct mechanisms of action and varied health implications.
Cocaine can be administered via snorting, injection, or smoking. It primarily functions by blocking the reuptake of dopamine, resulting in a euphoric high characterized by an intense sensation of happiness and...
Cocaine can be administered via snorting, injection, or smoking. It primarily functions by blocking the reuptake of dopamine, resulting in a euphoric high characterized by an intense sensation of happiness and...
01:25Adrenergic 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...
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...
01:31Adrenergic Antagonists: ɑ and β-Receptor Blockers
Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is clinically...