Event Title

Affects of Prenatal Food Deprivation on Offspring Microglial Morphology

Faculty Advisor

Sarah Cassella

Start Date

25-4-2017 4:00 PM

End Date

25-4-2017 5:00 PM

Description

Prenatal stress has shown to have adverse effects on various aspects of the developing brain, such as alterations in neuroendocrine functioning and neuroinflammatory processes. These changes may directly contribute to the development of psychiatric disorders such as addiction, anxiety, and schizophrenia. Psychiatric disease research has found an association between these disorders and altered immune function. The innate immune cells of the central nervous system are microglia, and they range in morphology from ramified with a surveying function, to amoeboid with a pro-inflammatory function. Neuroinflammation occurs when microglia accumulate and become active. We sought to determine if our prenatal stress model would induce neuroinflammation that would correlate with previously reported changes in neuroendocrine and behavioral outcomes. To model prenatal stress, we used a food deprivation paradigm (FD50) in which food was restricted by 50% during the second half (starting on E10) of pregnancy. We examined microglia in the relevant stress-related regions of the hippocampus and prefrontal cortex (PFC). Offspring brains were collected at postnatal day (P) 30 and P60 and microglial morphology was analyzed via soma area and branching complexity to determine differences in relative activation between male, female, control, and food restricted offspring. Ongoing analysis shows a significant increase in soma size between the control and restricted groups in only the infralimbic PFC, suggesting that these cells are functioning in a relatively activated state. Understanding the relationship between prenatal stress, inflammation and behavioral alterations could lead to enhanced prenatal care and therapies in the future.

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Apr 25th, 4:00 PM Apr 25th, 5:00 PM

Affects of Prenatal Food Deprivation on Offspring Microglial Morphology

Prenatal stress has shown to have adverse effects on various aspects of the developing brain, such as alterations in neuroendocrine functioning and neuroinflammatory processes. These changes may directly contribute to the development of psychiatric disorders such as addiction, anxiety, and schizophrenia. Psychiatric disease research has found an association between these disorders and altered immune function. The innate immune cells of the central nervous system are microglia, and they range in morphology from ramified with a surveying function, to amoeboid with a pro-inflammatory function. Neuroinflammation occurs when microglia accumulate and become active. We sought to determine if our prenatal stress model would induce neuroinflammation that would correlate with previously reported changes in neuroendocrine and behavioral outcomes. To model prenatal stress, we used a food deprivation paradigm (FD50) in which food was restricted by 50% during the second half (starting on E10) of pregnancy. We examined microglia in the relevant stress-related regions of the hippocampus and prefrontal cortex (PFC). Offspring brains were collected at postnatal day (P) 30 and P60 and microglial morphology was analyzed via soma area and branching complexity to determine differences in relative activation between male, female, control, and food restricted offspring. Ongoing analysis shows a significant increase in soma size between the control and restricted groups in only the infralimbic PFC, suggesting that these cells are functioning in a relatively activated state. Understanding the relationship between prenatal stress, inflammation and behavioral alterations could lead to enhanced prenatal care and therapies in the future.