Postnatal repeated maternal deprivation produces age-dependent changes of brain-derived neurotrophic factor

Mila Roceri1, Francesca Cirulli, Cassandra Pessina

  • 1Department of Pharmacological Sciences and Center of Excellence for Neurodegenerative Disorders, University of Milan, Milan, Italy.

Biological Psychiatry
|March 25, 2004
PubMed

Insights

Early life stress from maternal deprivation (MD) reduces brain-derived neurotrophic factor (BDNF) in adult brains, potentially increasing vulnerability to psychiatric disorders. This reduction may protect against further stress later in life.

Area of Science:

  • Neuroscience
  • Developmental Psychology
  • Molecular Psychiatry

Background:

  • Adverse early-life events can disrupt brain development and increase susceptibility to psychiatric disorders.
  • Understanding persistent neurobiological changes from early stress is key for developing new treatments.

Purpose of the Study:

  • To investigate the long-term effects of postnatal maternal deprivation (MD) on brain-derived neurotrophic factor (BDNF) levels.
  • To determine how MD impacts neurotrophin expression in the hippocampus and prefrontal cortex at different life stages.

Main Methods:

  • Postnatal repeated maternal deprivation (MD) was administered from postnatal day (PND) 2-14.
  • RNase protection assays and ELISA were used to measure neurotrophin expression.
  • Brain tissue from different ages, including adulthood, was analyzed.

Main Results:

  • MD caused a temporary increase in neurotrophin expression in the hippocampus and prefrontal cortex by PND 17.
  • In adulthood, MD led to a specific decrease in BDNF expression in the prefrontal cortex.
  • Adult MD animals showed reduced BDNF levels in the prefrontal cortex and striatum, unlike control animals under chronic swim stress.

Conclusions:

  • Maternal deprivation (MD) significantly reduces BDNF expression in the adult prefrontal cortex and striatum.
  • This reduction in BDNF may decrease neural plasticity, making these brain regions more vulnerable to stress.
  • The findings highlight a potential mechanism linking early-life stress to long-term psychiatric vulnerability.
Abstract

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