Mitochondria-Endoplasmic Reticulum Interaction in Central Neurons

Abstract

The proteins presenilin-1/2 play a key role in the interactions between mitochondria and the endoplasmic reticulum at synaptic contacts of central neurons. Several novel observations suggest that mutations in presenilin-1 lead to an abnormal energy state, an early sign of neurodegeneration and Alzheimer’s disease. Recent studies suggest that in the postsynaptic region, calcium stores are widely represented in the spine apparatus, which is located in a strategically important compartment - the neck of mature mushroom-shaped dendritic spines. Moreover, in the dendritic shaft area, at the base of the spines, one finds oblong mitochondrial clusters supplying the postsynaptic area and the local protein synthesis with ATP. Calcium signals, generated by the postsynaptic membranes, affect both calcium release from local stores through ryanodine channels and the uptake based on store-operated calcium entry. The entire complex of nanoscale signaling most likely determines the production of ATP. Violation of the functional relationship between mitochondria and reticular calcium depots can lead to disruption of signaling pathways that stimulate ATP production at the stages of increased activity of individual synapses. In this chapter, we will present the signaling mechanisms of interaction between mitochondria, spine clusters, and calcium nano-stores in postsynaptic area.