The control of dendritic branching by mitochondria

A fundamental difference between neurons in real brains and those in artificial neural networks is the way the neurons in each are connected. In artificial nets, the synapses between neurons often have adjustable strengths, but the structure and scale of the input dendritic field generally counts for little. For real neurons, where a “connection” between cells is not just a synapse but rather a whole net unto itself, structure and scale are everything. The architect of this dendritic structure is neither a DNA code nor a spontaneous developmental physics that condenses order from a protein-lipid chaos. This structure is in fact the byproduct of competitive, yet cooperative mitochondria that administer that code to themselves and to their host to control its interaction with other similarly controlled hosts.

Reseachers from Osaku University have found that if mitochondria are depleted from developing dendrites in pyramidal cells, there is increased branching in the proximal region of the dendrites. In their paper last week in the Journal of Neuroscience, they also show that these dendrites grow longer. Since mitochondria distribute not just energy but also metabolites, proteins, and mRNAs throughout the cell, these results may be somewhat surprising. However depending on what manipulations have been done to alter the mitochondria, many things might be expected to happen to dendrites and the cell in general.

Previous reports have shown that eliminating mitochondria from dendrites of mitofusion-2 null Purkinje cells results in a reduction in dendrite number. Other studies in cultured hippocampal neurons found no alterations in branch patterns. The present study achieved depletion of mitochondria from dendrites by altering similar mitofusion (Mfn) proteins. In this case Mfn-1 was overexpressed, essentially initiating a massive mitochondrial fusion fest. This subsequently confines them to the soma. The authors were also able to achieve the same effects on dendrites by overexpressing TRAK2. This is a truncated form of a motor-adapter protein which would presumably interfere with transport along the cytoskeleton.

The authors suggest that a main difference with their new study may be that for the prior Purkinje cell experiments the dendrites were already developed, while here the mitochondria were perturbed at the outset. They offer three mechanisms—ATP generation, Ca2 buffering, and caspase activation—towards an explanation of their observed effects, which unfortunately, they tend to simplify as being either “positive or negative dendritic regulation.” Via The control of dendritic branching by mitochondria.

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