Vitamin D Supporting Neurotransmitters!

Vitamin D was first proposed as a “possible” neurosteroid over 20 years ago due to the presence of specific vitamin D receptors in the brain and its effects on the developing and adult brain. More recently, it has been affirmed as a neurosteroid and dubbed “the neglected neurosteroid” by scientists closely studying its effects on brain development.

Numerous pathologies and brain disorders have been linked to vitamin D deficiency (e.g., schizophrenia, Parkinson’s, etc.). Regarding neurotransmission, there is strong evidence (experimental models are from cells and rodents) that vitamin D is important for the development and maintenance of dopamine signaling in the brain (the brain chemical most associated with motivation and reward-driven behavior). Note: there is cellular data suggesting that vitamin D deficiency may negatively affect the serotonergic system as well.

In developing brains, the vitamin D receptor can be found early, around the time most dopaminergic neurons are born. Vitamin D-deficient brains (rodents) have been shown to have a reduced number of specific proteins that are critical for the maturation of dopaminergic neurons (eliminating these proteins results in reduced numbers of dopaminergic cells and altered positioning of dopaminergic neurons – this has been shown to negatively affect dopamine metabolism later in life). Furthermore, another study showed that vitamin D deficiency in the developing brain results in reduced expression and protein levels of tyrosine hydroxylase (the rate-limiting enzyme for dopamine production). The same study demonstrated that these same brains had reduced levels of BDNF (another study showed reduced nerve growth factor) during critical developmental periods.

In models of neurodegeneration (in rodents), the active hormonal form of vitamin D protected and, in some cases, alleviated disease-specific pathology. For example, acute administration demonstrated protection of dopaminergic neurons in different Parkinson’s models (by increasing tyrosine hydroxylase activity).

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