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Prenatal stress-induced increases in hippocampal von Willebrand factor expression are prevented by concurrent
Gretchen N Neigh1, Christina L Nemeth2, Sean D Kelly3
1Department of Psychiatry and Behavioral Sci., Emory University, Atlanta, GA, USA; Department of Physiology, Emory University, Atlanta, GA, USA.
Insights
Prenatal stress impacts adult brain blood vessels, increasing von Willebrand factor. Escitalopram treatment during pregnancy may offer protection against these stress-induced cerebrovascular changes.
Area of Science:
- Neuroscience
- Cardiovascular Science
- Developmental Psychology
Background:
- Prenatal stress negatively affects neurological functions and adult health.
- Cerebrovascular health is crucial for neuronal function, yet prenatal stress effects are understudied.
- Vascular disturbances can lead to cerebral hypoperfusion, linked to neurodegenerative diseases.
Purpose of the Study:
- To investigate prenatal stress effects on cerebrovasculature, specifically von Willebrand factor and angiogenic factors.
- To assess if escitalopram treatment during prenatal stress exposure mitigates these cerebrovascular impacts.
- To examine the relationship between prenatal stress, cerebrovascular health, and adult stress responses.
Main Methods:
- Assessed von Willebrand factor and related angiogenic factors in response to prenatal stress.
- Evaluated the impact of concurrent escitalopram treatment during prenatal stress.
- Measured total vascularization, blood vessel length, and hippocampal reactive oxygen species production in adulthood.
Main Results:
- Prenatal stress increased von Willebrand factor expression, an effect blocked by escitalopram.
- Adult chronic stress decreased blood vessel length, but prenatal stress did not affect total vascularization.
- Prenatal escitalopram exposure reduced hippocampal reactive oxygen species production.
Conclusions:
- Prenatal stress induces complex changes in adult cerebral vascular structure and function.
- In utero escitalopram treatment may offer protective effects against prenatal stress-induced cerebrovascular alterations.
- The findings highlight the long-term impact of the prenatal environment on brain vasculature and health.
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.
