However, we assume that the decrease in the Pax2 expression may be associated with the inhibitory effect of Pax6, with its expression, vice versa, increasing significantly after a traumatic injury

However, we assume that the decrease in the Pax2 expression may be associated with the inhibitory effect of Pax6, with its expression, vice versa, increasing significantly after a traumatic injury. The obtained data raise various questions to address in the further study of neurogenesis in the adult Pacific salmon brain as follows. lateral (Dl), medial (Dm) zones of the pallium, and the lateral zone (Vl) of the subpallium compared to the control. We believe that the decrease in the expression of Pax2 may be caused by the inhibitory effect of the Pax6 transcription factor, whose expression in the Danshensu juvenile salmon brain increases upon injury. [4], the catfish [5], and masu salmon [6]. However, it still remains unclear what signaling mechanisms are involved in the activation of adult neural stem cells after damage (reactive proliferation) and in the production of new neurons (regenerative neurogenesis) from progenitor cells. The central nervous system (CNS) in fishes and amphibians has the highest capacity for neurogenesis, with the physiological neurogenesis and transdifferentiation of pre-existing elements launched simultaneously after a traumatic injury [7]. The physiological and regenerative neurogenesis in reptiles has not yet been sufficiently elucidated [8]. Rabbit polyclonal to FOXO1A.This gene belongs to the forkhead family of transcription factors which are characterized by a distinct forkhead domain.The specific function of this gene has not yet been determined; However, the results of studies on the medial cortex in the leopard gecko show the presence of proliferating pools of neural stem/progenitor cells in the demonstrated sharply increasing the number of CBS+ cells after 3 days, which indicates the involvement of H2S in the post-traumatic response [16]. Similar results were observed after optic nerve injury in trout, which showed a significant increase in the number of H2S-producing cells in the integrative centers of the brain: telencephalon, optic tectum, and cerebellum [17]. A noteworthy finding was the presence of CBS-producing radial glia in the optic tectum of trout after the optic nerve injury [18]. H2S has a significant effect on physiological and pathophysiological processes in the CNS, being involved in protective mechanisms induced by traumatic brain injury (TBI) and ischemic reperfusion [19]. Acute inflammation in mammals typically has a negative effect on neurogenesis and regeneration by promoting glial scar formation and inhibiting the proliferation of progenitor cells, as well as the migration, survival, maturation, and integration of Danshensu new neurons [20,21]. The inflammatory response observed at the site of injury in the fish brain after TBI, on the contrary, did not limit neuronal regeneration [3,12]. Currently, the involvement of H2S in the processes of ischemic brain injury, TBI and the involvement of this gas transmitter in the control of oxidative stress and the increase in reactive oxygen species in the H2S-dependent signaling are being actively studied [19,22,23]. H2S reactions with many signaling mediators, transcription factors, and channel proteins are known to occur in neurons and glial cells both in vivo and in vitro [14,19]. However, information on the intercellular interaction and the involvement of H2S in regenerative processes, in particular, in adult neurogenesis and TBI, is still limited. Adult neurogenesis and neuronal regeneration after injury are controlled by the activation of certain molecular pathways, including transcription factors, growth factors, neurotrophins, and cytokines, which are expressed in certain neurogenic niches and, ultimately, at the damaged CNS site. Shh signaling plays an important role in both CNS neurogenesis and regeneration [24]. Transcription factors of the Paired Box (PAX) family are one of the factors regulated by the Shh signaling pathway; however, the mechanisms regulating the Pax2 expression are almost unstudied [25]. Studies on trout have shown that damage Danshensu to the optic nerve leads to an increase in the number of Pax2+ reactive astrocytes in it, being involved in the initial stages of the optic nerve axon regeneration [26]. In the case of optic nerve Danshensu injury, a significant increase in the number of Pax6+ cells has been revealed in the parts of the trout brain that have directed retinal inputs (the visual nuclei of the diencephalon and the optic tectum) [27]. It has been found that some of the Pax6+ cells have a neuroepithelial phenotype and are part of reactive neurogenic niches located in the periventricular zone (PVZ) and parenchymal regions of the brain. Another population of Pax6+ cells has a radial glia phenotype and arises as a result of activation of constitutive neurogenic domains, as well as within newly formed reactive neurogenic niches [26]. Juvenile Pacific salmon is a convenient model for.