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AMPK activation prevents prenatal stress-induced cognitive impairment: modulation of mitochondrial content and

Ke Cao1, Adi Zheng1, Jie Xu1

  • 1Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology and Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, China.

Free Radical Biology & Medicine
|August 6, 2014
PubMed

Insights

Prenatal stress impairs offspring cognition, linked to mitochondrial issues. Maternal resveratrol supplementation activates AMP-activated protein kinase (AMPK), improving mitochondrial function and cognitive outcomes in offspring.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Prenatal stress is linked to offspring cognitive deficits.
  • Mitochondrial dysfunction and oxidative stress are implicated in these deficits.
  • The role of AMP-activated protein kinase (AMPK) pathway in this context is under investigation.

Purpose of the Study:

  • To investigate the involvement of the AMPK pathway in prenatal stress-induced cognitive impairment.
  • To determine if resveratrol (Res), an AMPK activator, can prevent these impairments.
  • To explore the mechanisms underlying Res's effects, including mitochondrial biogenesis and oxidative stress modulation.

Main Methods:

  • In vitro studies using SH-SY5Y cells treated with Res and Compound c (AMPK inhibitor).
  • In vivo studies using a prenatal restraint stress (PRS) animal model with maternal Res supplementation.
  • Assessment of mitochondrial biogenesis, phase II enzyme activation, protein oxidation, and oxidative damage.
  • Evaluation of cognitive function using spontaneous alternation performance and Morris water maze tests.
  • Analysis of neuron marker mRNA levels and hippocampal AMPK activation.

Main Results:

  • Res treatment in cells increased mitochondrial biogenesis and phase II enzymes, reduced oxidative stress markers, effects abolished by Compound c.
  • Maternal Res supplementation in PRS model activated hippocampal AMPK in offspring.
  • Res inhibited PRS-induced mitochondrial loss and oxidative damage in offspring hippocampi.
  • Res improved PRS-induced deficits in neuron marker expression and cognitive function in offspring.
  • Res activated Nrf2-mediated phase II enzymes in offspring.

Conclusions:

  • AMPK activation by Res plays a crucial role in preventing prenatal stress-induced cognitive impairment.
  • AMPK modulates mitochondrial content and phase II enzymes in neuronal cells.
  • The coupling of mitochondrial biogenesis and the Nrf2 pathway via AMPK may be a therapeutic target for neurological disorders.

Keywords:
AMPKCognitive functionMitochondrial biogenesisOxidative stressPrenatal stressResveratrol

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