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Author Notes:

Gretchen N. Neigh, Department of Anatomy & Neurobiology, Virginia Commonwealth University, PO Box 980709, Richmond, VA 23298, USA, Email: gretchen.mccandless@vcuhealth.org.

MJO serves as a consultant to H. Lundbeck and receives compensation for these services.

The terms of this arrangement have been reviewed and approved by Emory University in accordance with its conflict of interest policies.

Subjects:

Research Funding:

This work was funded by the following grants from the National Institutes of Health: MH-077928 to ZNS.

This study was supported in part by the Emory University School of Medicine Integrated Cellular Imaging Microscopy Core and the Emory Neuroscience NINDS Core Facilities grant (P30NS055077).

Keywords:

  • Escitalopram
  • Prenatal stress
  • Reactive oxygen species
  • Stress
  • Vascular length
  • Von Willebrand factor
  • Age Factors
  • Amygdala
  • Angiogenic Proteins
  • Animals
  • Citalopram
  • Female
  • Hippocampus
  • Male
  • Prefrontal Cortex
  • Pregnancy
  • Prenatal Exposure Delayed Effects
  • Rats
  • Reactive Oxygen Species
  • Stress, Psychological
  • von Willebrand Factor

Prenatal stress-induced increases in hippocampal von Willebrand factor expression are prevented by concurrent prenatal escitalopram

Tools:

Journal Title:

Physiology and Behavior

Volume:

Volume 172

Publisher:

, Pages 24-30

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Prenatal stress has been linked to deficits in neurological function including deficient social behavior, alterations in learning and memory, impaired stress regulation, and susceptibility to adult disease. In addition, prenatal environment is known to alter cardiovascular health; however, limited information is available regarding the cerebrovascular consequences of prenatal stress exposure. Vascular disturbances late in life may lead to cerebral hypoperfusion which is linked to a variety of neurodegenerative and psychiatric diseases. The known impact of cerebrovascular compromise on neuronal function and behavior highlights the importance of characterizing the impact of stress on not just neurons and glia, but also cerebrovasculature. Von Willebrand factor has previously been shown to be impacted by prenatal stress and is predictive of cerebrovascular health. Here we assess the impact of prenatal stress on von Willebrand factor and related angiogenic factors. Furthermore, we assess the potential protective effects of concurrent anti-depressant treatment during in utero stress exposure on the assessed cerebrovascular endpoints. Prenatal stress augmented expression of von Willebrand factor which was prevented by concurrent in utero escitalopram treatment. The functional implications of this increase in von Willebrand factor remain elusive, but the presented data demonstrate that although prenatal stress did not independently impact total vascularization, exposure to chronic stress in adulthood decreased blood vessel length. In addition, the current study demonstrates that production of reactive oxygen species in the hippocampus is decreased by prenatal exposure to escitalopram. Collectively, these findings demonstrate that the prenatal experience can cause complex changes in adult cerebral vascular structure and function.

Copyright information:

© 2016 Elsevier Inc.

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