Recently, a study found that activated neurons can release a kind of “mysterious” proteins to protect nerve cells from death threats. The latest study, conducted by researchers led by the University of Heidelberg in Germany, is published in international academic journal Cell Reports.
Professor Bading, who led the study, said that, we already know by enhancing brain activity that we can promote the protective effect on neurons, but now we have found a key mechanism to facilitate this process, but also found a nerve protective molecules produced by the body.
Early studies led by Professor Bading has found that brain activity is able to combat nerve cell death, and NMDA receptor plays an important role in the molecular level. This receptor is a molecule that is activated by neurotransmitter; when stimulated, NMDA receptor will lead calcium ions into the cell and into the nucleus; the calcium signal propagation will launch a series of protective gene expression within the cell. But how exactly this process plays a protective role remains unclear.
In this latest study, the researchers found the answer by studying the NMDA receptor. They found that if the receptor molecule is not located at the nerve connections (such as synapses), they will not be able to protect the cells, and they also cause serious damages to the nerve cells, leading to cell death. The increased brain activity can inhibit toxicity of NMDA receptors outside the synapse. Researchers have found that activin A ( Inhibin β-A) is a key protein in the activation of this process.
Activin A plays an important role in the female menstrual cycle and wound healing. Neuronal activity can stimulate the nervous system to produce Activin A, which causes reduction of synaptic NMDA receptors outside the synapses, so as to establish a protection “shield” for cells, in addition, Activin A also exert a protective mediated BDNF activity. So we can say that Activin A is the key activating factor for brain neuroprotective mechanisms. The study provides new possibilities for the development of neurodegenerative diseases strategy.
Source: BDNF Reduces Toxic Extrasynaptic NMDA Receptor Signaling via Synaptic NMDA Receptors and Nuclear-Calcium-Induced Transcription of inhba/Activin A, Cells Reports.