Nama : Sintia
Widyo Wati
NPM : 2A214304
Kelas : 3EB24
NPM : 2A214304
Kelas : 3EB24
Vitamin D and Depression: Cellular and Regulatory
Mechanisms
Michael
J. Berridge
Eric
L. Barker, ASSOCIATE EDITOR
Pharmacological
Reviews April 2017, 69 (2) 80-92; DOI: https://doi.org/10.1124/pr.116.013227
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Abstract
Depression
is caused by a change in neural activity resulting from an increase in
glutamate that drives excitatory neurons and may be responsible for the decline
in the activity and number of the GABAergic inhibitory neurons. This imbalance
between the excitatory and inhibitory neurons may contribute to the onset of
depression. At the cellular level there is an increase in the concentration of
intracellular Ca2+ within the inhibitory neurons that is driven by an increase
in entry through the NMDA receptors (NMDARs) and through activation of the
phosphoinositide signaling pathway that generates inositol trisphosphate
(InsP3) that releases Ca2+ from the internal stores. The importance of these
two pathways in driving the elevation of Ca2+ is supported by the fact that
depression can be alleviated by ketamine that inhibits the NMDARs and
scopolamine that inhibits the M1 receptors that drive InsP3/Ca2+ pathway. This
increase in Ca2+ not only contributes to depression but it may also explain why
individuals with depression have a strong likelihood of developing Alzheimer’s
disease. The enhanced levels of Ca2+ may stimulate the formation of Aβ to
initiate the onset and progression of Alzheimer's disease. Just how vitamin D
acts to reduce depression is unclear. The phenotypic stability hypothesis
argues that vitamin D acts by reducing the increased neuronal levels of Ca2+
that are driving depression. This action of vitamin D depends on its function
to maintain the expression of the Ca2+ pumps and buffers that reduce Ca2+
levels, which may explain how it acts to reduce the onset of depression.
Footnotes
dx.doi.org/10.1124/pr.116.013227.
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