Generating brain power where it is needed
Generating brain power where it’s needed
16 March 2009
MRC funded scientists led by Dr Josef Kittler at UCL (University College London) have identified how a protein called Miro1 helps match energy supply to energy use in brain cells. The finding helps explain why mental and physical damage can occur after the brain has been starved of energy, for example if a person suffers a stroke.
Information flows along and between nerve cells in the brain as electrical signals. The signals are generated by charged atoms (ions) flooding into the cells to pass on the message. Pumping the ions back out of the nerve cells again uses up most of the brain’s energy supply. A trauma to the nervous system like stroke or spinal cord injury causes a deficit of energy, producing nerve cell damage that can in turn lead to mental or physical disability.
Energy is generated within cells by organelles, smaller cell units, called mitochondria. The junctions between nerve cells, known as synapses, are sites of huge energy consumption that need to be able to attract the mitochondria required to keep signals going. In a paper published in the journal Neuron, Dr Kittler reveals how the protein Miro1 helps to guide mitochondria to the synapses.
Dr Kittler explains: ‘‘Mitochondria can be moved around cells by small motors, on intracellular protein tracks called microtubules. The linkage of mitochondria to these motors is mediated by Miro1. The link between the mitochondria and the motor keeping it on the microtubule track is broken, or uncoupled, by the ions of calcium that help to regulate many cell functions. When a nerve cell is activated by an electric signal, and so asked to pass on information, the calcium ions enter the cell. This causes the mitochondria to break away from the motor and be ‘parked’ next to the synapses where energy is needed.’’
The research is a good example of how understanding the way that tiny, but crucial, cell components like the mitochondria work contributes to understanding problems that affect whole body systems.
Dr Kittler concludes: ‘‘This work advances our understanding of how nerve cells in the brain are powered. It also explains why in pathological conditions like stroke, which dramatically raise the internal calcium concentration in nerve cells, all movements of mitochondria within the cell halt.’’
For more information about Dr Kittler’s research including images and video please visit his webpage.
Original research paper: MIRO1 is a calcium sensor for glutamate receptor dependent localization of mitochondria at synapses is published in Neuron:
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