Related Experiment Video

Updated: Aug 14, 2026

Assessment and Evaluation of the High Risk Neonate: The NICU Network Neurobehavioral Scale
19:15

Assessment and Evaluation of the High Risk Neonate: The NICU Network Neurobehavioral Scale

Published on: August 25, 2014

Prenatal impairment of brain serotonergic transmission in infants

Gabriel Manjarrez1, Ignacia Cisneros, Rocio Herrera

  • 1Laboratory of Developmental Neurochemistry, Specialties Hospital, XXI Century National Medical Center, Mexican Institute of Social Security, Av. Cuauhtémoc 330, Col. Doctores, CP 06720, Mexico City, Mexico. willisga@df1.telmex.net.mx

The Journal of Pediatrics
|November 18, 2005
PubMed

Insights

In infants with intrauterine growth restriction (IUGR), elevated free L-tryptophan (L-Trp) correlated with reduced auditory evoked potentials (AEPs), suggesting impaired brain serotonin activity.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Developmental Pediatrics

Background:

  • Intrauterine growth restriction (IUGR) is linked to altered neurodevelopment.
  • Serotonin plays a crucial role in brain development and function.
  • Auditory evoked potentials (AEPs) can reflect neural pathway integrity.

Purpose of the Study:

  • To investigate the relationship between free L-tryptophan (L-Trp) levels and auditory evoked potentials (AEPs) in infants with IUGR.
  • To assess if these parameters indicate impaired brain serotonin neurotransmission.

Main Methods:

  • A prospective, longitudinal study compared infants with IUGR to control infants.
  • Measured free, bound, and total plasma L-tryptophan.
  • Recorded the N1/P2 component of AEPs.

Main Results:

  • Infants with IUGR exhibited higher plasma free L-Trp levels compared to controls.
  • A significant decrease in the amplitude of the N1/P2 AEP component was observed in IUGR infants.
  • A negative association was found between free L-Trp fraction and N1/P2 AEP amplitude.

Conclusions:

  • Elevated free L-Trp and reduced N1/P2 AEP amplitude in IUGR newborns suggest an inverse relationship.
  • These alterations may indicate impaired in utero brain serotonergic activity.
  • Epigenetic factors and serotonin metabolism disturbances in IUGR might influence sensory cortex development and adult serotonin-related disorders.
Abstract

More Related Videos

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders19:57

The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders

Published on: August 5, 2017

Related Concept Videos

Teratogenicity01:07

Teratogenicity

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...
Gut-Brain Axis01:22

Gut-Brain Axis

The gut–brain axis is a bidirectional communication system that connects the gastrointestinal tract and the brain. This interaction is mediated through multiple pathways, including the vagus nerve, hormonal signals, immune responses, and chemical messengers produced by gut microbes.Microbial Contributions to Brain FunctionGut microbiota contributes significantly to brain function by producing neuroactive compounds. These include neuroactive compounds that influence neurotransmitters such as...
Biological Causes of Schizophrenia01:29

Biological Causes of Schizophrenia

Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin studies.
G-protein Coupled Receptors01:21

G-protein Coupled Receptors

G-protein coupled receptors are ligand binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that transverses the cell membrane seven times creating intracellular and extracellular loops. The extracellular loops create a ligand specific pocket which binds to neurotransmitters or hormones. The intracellular loops holds onto the G-protein.