Mitochondria and Neuroplasticity

Abstract

The production of neurons from neural progenitor cells, the growth of axons and dendrites and the formation and reorganization of synapses are examples of neuroplasticity. These processes are regulated by cell-autonomous and intercellular (paracrine and endocrine) programs that mediate responses of neural cells to environmental input. Mitochondria are highly mobile and move within and between subcellular compartments involved in neuroplasticity (synaptic terminals, dendrites, cell body and the axon). By generating energy (ATP and NAD+), and regulating subcellular Ca2+ and redox homoeostasis, mitochondria may play important roles in controlling fundamental processes in neuroplasticity, including neural differentiation, neurite outgrowth, neurotransmitter release and dendritic remodelling. Particularly intriguing is emerging data suggesting that mitochondria emit molecular signals (e.g. reactive oxygen species, proteins and lipid mediators) that can act locally or travel to distant targets including the nucleus. Disturbances in mitochondrial functions and signalling may play roles in impaired neuroplasticity and neuronal degeneration in Alzheimer's disease, Parkinson's disease, psychiatric disorders and stroke.

Mitochondrial function in the brain links anxiety with social subordination

“…S4B and Table S1). Mitochondrial respiratory function is essential for neural processing, as it plays key roles in many essential functions required for neural homeostasis and computations (24)(25)(26). Thus, we reasoned that the disadvantage of high-anxious rats to win the competition against lowanxious rats could reflect a lower mitochondrial activity in the NAc.…”

Weight of evidence evaluation of a network of adverse outcome pathways linking activation of the nicotinic acetylcholine receptor in honey bees to colony death

“…It has been reported that a single neuron in the human brain can consume~4.7 billion ATP molecules per second (Nicholls and Budd, 2000). Therefore, a continuous source of mitochondrial ATP is essential for neuronal function and synaptic plasticity (Cheng et al, 2010). As described as a component of the normal biology for KE3, the mitochondria is directly involved in supplying ATP to AC for conversion to cAMP, which acts as a second messenger involved in the signaling pathway leading to CREB/CRE activation (Fig.…”

Mitochondria and the central nervous system: searching for a pathophysiological basis of psychiatric disorders

“…These changes may include mitochondrial Ca 2+ uptake or release, production of superoxide and other ROS, and release of proteins and other factors. 13 …”

“…[11][12][13] Several prominent signaling pathways that stimulate mitochondrial biogenesis and energy metabolism, while simultaneously regulating neuroplasticity, have been demonstrated. 13 Mitochondria are distributed throughout the length of axons and presynaptic terminals. In addition, they are found in dendrite shafts and associated with dendritic spines.…”

“…They have tree-like shapes, are electrically excitable, and act in signal detection, integration, and storage, as well as in the generation of adaptive responses. 13 Through the use of imaging and molecular biology techniques for the study of mitochondria, several surprising properties and functions of mitochondria in neuroplasticity have been revealed. Mitochondria move rapidly within and between subcellular compartments 16 ; undergo fission and fusion 17 ; respond (e.g., move, change their energy output, take up or release calcium) to electrical activity and activation of neurotransmitters and growth factor receptors 18 ; and function as signaling outposts that contain kinases, deacetylases, and other signal transduction enzymes.…”