Writing in the journal Cell, researchers from The Scripps Research Institute (TSRI) in Florida, discovered that blocking a channel that brings calcium to the mitochondria causes memory impairment in fruit flies. However this action did not seem to alter learning capacity.
The mitochondrion is considered the powerhouse of a cell. This organelle produces most of the cell's adenosine triphosphate (ATP), a source of chemical energy.
The findings give new insights into calcium’s role in the mitochondria and the effects a diet low in calcium could potentially cause.
In humans calcium is crucial for vascular contraction and vasodilation, muscle function, nerve transmission, intracellular signalling and hormonal secretion.
Current daily intake of calcium as recommended by the European Food Safety Authority (EFSA) place a tolerable upper intake level (UL) of 2,500 mg of calcium per day from all sources for adults and pregnant and lactating women.
Fruit fly observations
Lead by Ron Davis, chair of the Department of Neuroscience at Scripps Florida, the team showed that in fruit flies, inhibiting the mitochondrial calcium uniporter, during pupation (a mid-life stage of insects undergoing transformation) memory was impaired – an observation not found during adulthood.
The team thought this was associated with structural defects in the specific brain region (MBn) critical for memory formation.
This was exacerbated by a decrease in synaptic vesicles and an increased length in the axons of this brain region.
“The new study’s conclusion is that mitochondrial calcium entry during development is necessary to establish the neuronal competency for supporting adult memory,” said TSRI research associate Ilaria Drago, one of the authors of the study.
Previous studies have shown that the mitochondrial calcium uniporter protein is regulated by the proteins MICU1, MICU2 and EMRE.
Human patients with mutations in MICU1 can exhibit learning disabilities.
“Overall, the results dictate the conclusion that uniporter function in developing MBn establishes the neurons’ competence to support adult memory by participating in processes that provide proper neuronal structure, physiology, and/or circuitry,” the study discussed.
The team acknowledged that it was difficult to draw a strict correlation between MICU1 function, calcium entry into mitochondria and cognition.
They gave a range of explanations for their observations including the type of cellular stimulation used, possible differences in the uniporter complex.
“Additional studies are required to resolve the basis for these differences,” the study suggested.
“Our study thus offers guidance in further pursuit of understanding mitochondrial uniporter function, neuronal development, and adult cognition.”
Published online ahead of print: doi.org/10.1016/j.celrep.2016.08.017
“Inhibiting the Mitochondrial Calcium Uniporter during Development Impairs Memory in Adult Drosophila.”
Authors: I. Drago and R. Davis