Researchers have revealed how mitochondria play a crucial role in controlling the rejuvenation of tissues and synaptic plasticity in the adult mouse brain. Nerve cells, also known as neurons, are one of the most intricate types of cells in the human body. They develop their complexity by extending branched structures called dendrites and axons, and forming thousands of synapses to create complex networks. While most neurons are produced during embryonic development, there are a few regions of the brain that continue to generate new neurons throughout adulthood. The process of how these newly born neurons mature and compete successfully is still not fully understood.The functions of cells within a fully developed organ are crucial. However, comprehending these processes could be beneficial for treating brain diseases.
Professor Dr. Matteo Bergami and a team of researchers from the University of Cologne’s CECAD Cluster of Excellence in Aging Research conducted a study with mouse models to investigate this issue. They utilized imaging, viral tracing, and electrophysiological techniques and discovered that as new neurons mature, their mitochondria (the cells’ power houses) along dendrites undergo an increase in fusion dynamics to take on more elongated shapes. This process is essential for sustaining the health and function of the brain.The study ‘Enhanced mitochondrial fusion during a critical period of synaptic plasticity in adult-born neurons’ has been published in the journal Neuron. This study explores the plasticity of new synapses and the refinement of pre-existing brain circuits in response to complex experiences. The findings suggest that mitochondrial fusion grants new neurons a competitive advantage. Adult neurogenesis occurs in the hippocampus, a brain region that controls aspects of cognition and emotional behavior. Changes in the rates of hippocampal neurogenesis have been linked to neurodegenerative and depressive disorders. This study sheds light on the important role of mitochondrial fusion in the development of new neurons.Newly formed neurons in this area take a long time to mature to ensure the tissue remains highly flexible, but we don’t know much about how this happens. Bergami and his team found that the speed at which mitochondria fuse in the dendrites of these new neurons affects their flexibility at synapses, rather than just the maturation of the neurons themselves.
“We were surprised to find that new neurons can develop almost perfectly even without mitochondrial fusion, but their survival suddenly drops without any obvious signs of degeneration,” Bergami said. “This suggests that fusion plays a role in controlling the health of the neurons.”The process of petition at synapses is a crucial part of the selection process for new neurons as they integrate into the network. These findings further our understanding of how dysfunctional mitochondrial dynamics, such as fusion, can lead to neurological disorders in humans. It also suggests that fusion may have a more intricate role in controlling synaptic function and its malfunction in diseases like Alzheimer’s and Parkinson’s than previously believed. In addition to uncovering a fundamental aspect of neuronal plasticity in normal conditions, the scientists are optimistic that these results will help guide them toward interventions to restore neuronal plasticity.The article discusses the relationship between mitochondrial fusion, synaptic plasticity, and cognitive functioning in the context of disease.
