1,25-Dihydroxyvitamin D3 treatment results in increased choline acetyltransferase activity in specific brain nuclei.
Level 5 - mechanism / opinion, no new human data
Preclinical animal research
PubMed 3753932 · doi:10.1210/endo-118-4-1433
What was done
Researchers measured calcium-binding protein (CaBP) levels, choline acetyltransferase (CAT) activity, and monoamine oxidase activity in discrete brain nuclei of vitamin D-deficient male rats compared to rats repleted with 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. Repletion protocols included 8 daily intraperitoneal (IP) injections (100 or 200 ng) or 7-day continuous intraventricular (IVI) infusion (25 ng/day). Control infusions included IVI calcium (2 mM) or 25-hydroxyvitamin D3 (125 ng/day). Serum testosterone and luteinizing hormone (LH) were also assayed.
What was found
Repletion with 1,25-(OH)2D3 via IP or IVI routes significantly increased CAT activity in the arcuate-median eminence and the bed nucleus of the stria terminalis by 12% to 45% in a dose-dependent manner. IVI calcium or 25-hydroxyvitamin D3 produced no CAT changes. Monoamine oxidase and CaBP levels remained unchanged across brain nuclei. Vitamin D-deficient rats had abnormally low serum testosterone, which increased 2- to 5-fold to normal levels after 1,25-(OH)2D3 treatment, with parallel increases in serum LH.
Why it matters
These findings suggest that active vitamin D regulates central cholinergic enzyme activity in specific hypothalamic and limbic regions and contributes to the neuroendocrine control of gonadal hormones.
Limits
The study was conducted entirely in male rats, and sample sizes per group were not reported in the abstract. Findings cannot be directly extrapolated to human physiology without clinical verification.
Cited by
- supports Vitamin D produces or upregulates the enzyme that synthesizes acetylcholine.
- supports When vitamin D binds its nuclear receptor, it stimulates the expression of choline acetyltransferase, the enzyme that synthesizes acetylcholine.