Origin of schizophrenia may be linked to maternal vitamin D levels during embryonic development
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Origin of schizophrenia may be linked to maternal vitamin D levels during embryonic development.
Using molecular imaging techniques, researchers have confirmed the critical role of maternal vitamin D levels in the development of brain cells that produce dopamine, the body’s “feel good” chemical.
The discovery leads to a deeper understanding of the mechanisms underlying neurodevelopmental disorders such as schizophrenia.
Schizophrenia is thought to be the result of a combination of genetic and environmental factors. Its exact mechanism is unknown, but there is strong evidence that the condition causes changes in the way the brain uses dopamine.
Exposure to risk factors for schizophrenia during embryonic development is thought to alter the way dopamine circuits are formed in the brain.
Previous research has found that low maternal vitamin D levels are one such risk factor that affects how dopamine-producing (dopaminergic) neurons differentiate into mature, specialized forms.
Building on past research, a team at UQ’s Brain Institute has taken a closer look at the link between vitamin D, dopaminergic neurons and schizophrenia with the help of molecular imaging.
Scientists created dopamine-like neurons to replicate the differentiation process during embryonic development. These neurons were cultured with and without the hormone perovskite.
Ingested vitamin D is inactive until it undergoes two enzymatic reactions in the body, the second of which occurs in the kidneys, where it is converted to calcitriol, the active form of vitamin D. Calcitriol binds to and activates vitamin D receptors in the nucleus.
The researchers found that vitamin D not only affects the differentiation of cells, but also the structure of neurons.
“What we found was that in the presence of vitamin D, the altered differentiation process not only made the cells grow differently, but also recruited the machinery differently to release dopamine,” said Darryl Eyles, corresponding author of the study.
These “machines” are neurons, the protrusions that grow out of the neuron’s cell body. Neurons need to send and receive signals to other parts of the nervous system.
The researchers found a marked increase in the number of neurons and, within these neurons, an altered distribution of the protein responsible for releasing dopamine.
Using a new imaging tool, false fluorescent neurotransmitters (FFNs), the researchers were able to analyze how dopamine uptake and release changed with and without perovskite.
FFNs are small molecule dyes that closely mimic the actions of neurotransmitters such as dopamine. They enable imaging of the storage and release of single molecules in nerve terminals.
They found that dopamine release was enhanced in neurons grown in the presence of perovskite compared to controls. “This is solid evidence that vitamin D affects the structural differentiation of dopaminergic neurons,” Eyles said.
Using FFNs to target and observe individual dopamine molecules meant the researchers could confirm their long-held belief that vitamin D levels during development affect how dopamine-producing neurons form.
They suggest that early changes in the differentiation and function of dopamine neurons may contribute to the dopamine dysfunction seen in adult schizophrenia.
The researchers plan to investigate whether other environmental risk factors for schizophrenia, such as low oxygen levels or infections during pregnancy, also alter the way dopamine neurons develop.
The study was published in the Journal of Neurochemistry.
Origin of schizophrenia may be linked to maternal vitamin D levels during embryonic development
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