In the Special issue, we would like to consider the actual issues of adult and reparative neurogenesis and the expected means of regulating these processes and participation of neurochemical intercellular signaling in spatio-temporal organization of these processes. Currently, great attention concentrated on a questions about interaction of nervous and immune systems and the involvement of these systems in the organization of inflammatory responses after brain and spinal cord injuries. Interesting and relevant techniques are in vivo video monitoring of immune system´s cells, involved in the inflammatory response after trauma of CNS. Speed of the cellular response in traumatic brain injuries determinates by the relationship between proliferation and apoptosis. Efficiency of repair processes associated with the process of elimination and disposal of damaged cells in brain´s centers or pathways. Factors of neuroprotection are other relevant substances, which protect cells from the toxic effects of inflammatory mediators and therefore contribute to a more rapid recovery of damaged areas of CNS. Gaseous mediators, such as NO, H2S and CO have low molecular weight and play a major role in intercellular communications during reparative processes and traumatic injury. Their broad regulatory influence extends to various aspects of the functional activity of central nervous system in normal conditions and after damaged influence. Particular attention in this issue will be paid to morphogenetic influence of such agents. As a result of adult and reparative neurogenesis in proliferative areas of brain generated various types of cells, including neurons. The rate of generation of new neurons in proliferative areas of brain determines the effectiveness of reparative neurogenesis. Exploration of new regenerative-associated factors involved in the production of new cells in the adult brain and determine the success of the repair in regenerative competent organisms for understanding of mechanisms these processes have great importance.