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Adult neurogenesis is a complex, presumably conserved phenomenon in vertebrates with a broad range of variations regarding neural progenitor/stem cell niches, cellular composition of these niches, migratory patterns of progenitors and so forth among different species. Current understanding of the reasons underlying the inter-species differences in adult neurogenic potential, the identification and characterization of various neural progenitors, characterization of the permissive environment of neural stem cell niches and other important aspects of adult neurogenesis is insufficient. In the last decade, zebrafish has emerged as a very useful model for addressing these questions. In this review, we have discussed the present knowledge regarding the neural stem cell niches in adult zebrafish brain as well as their cellular and molecular attributes. We have also highlighted their similarities and differences with other vertebrate species. In the end, we shed light on some of the known intrinsic and extrinsic factors that are assumed to regulate the neurogenic process in adult zebrafish brain. © 2017 Wiley Periodicals, Inc. Develop Neurobiol 77: 1188-1205, 2017.

Brain‐derived neurotrophic factor (BDNF) is an extensively studied protein that is evolutionarily conserved and widely distributed in the brain of vertebrates. It acts via its cognate receptors TrkB and p75NTR and plays a central role in the developmental neurogenesis, neuronal survival, proliferation, differentiation, synaptic plasticity, learning and memory, adult hippocampal neurogenesis, and brain regeneration. BDNF has also been implicated in a plethora of neurological disorders. Hence, understanding the processes that are controlled by BDNF and their regulating mechanisms is important. Although, BDNF has been thoroughly studied in the mammalian models, contradictory effects of its functions have been reported on several occasions. These contradictory effects may be attributed to the sheer complexity of the mammalian brain. The study of BDNF and its associated functions in a simpler vertebrate model may provide some clarity about the effects of BDNF on the neurophysiology of the brain. Keeping that in mind, this review aims at summarizing the current knowledge about the distribution of BDNF and its associated functions in the zebrafish brain. The main focus of the review is to give a comparative overview of BDNF distribution and function in zebrafish and mammals with respect to distinct life stages. We have also reviewed the regulation of bdnf gene in zebrafish and discussed its role in developmental and adult neurogenesis.

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In the recent years, zebrafish, owing to its tremendous adult neurogenic capacity, has emerged as a useful vertebrate model to study brain regeneration. Recent findings suggest a significant role of the BDNF/TrkB signaling as a mediator of brain regeneration following a stab injury in the adult zebrafish brain. Since BDNF has been implicated in a plethora of physiological processes, we hypothesized that these processes are affected in the injured zebrafish brain. In this small study, we examined the indicators of oxidative stress and of apoptosis using biochemical assays, RT-PCR and IHC to reflect upon the impact of stab injury on oxidative stress levels and apoptosis in the injured adult zebafish brain. Our results indicate induction of oxidative stress in the injured adult zebrafish brain. Also, apoptosis was induced in the injured brain as indicated by increased protein levels of cleaved caspase3 as well as enhanced mRNA levels of both pro-apoptotic and anti-apoptotic genes. This knowledge contributes to the overall understanding of adult neurogenesis in the zebrafish model and raises new questions pertaining to the compensatory physiological mechanisms in response to traumatic brain injury in the adult zebrafish brain.

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In the recent years, zebra sh, owing to its tremendous adult neurogenic capacity, has emerged as a useful vertebrate model to study brain regeneration. Recent ndings suggest a signi cant role of the BDNF/TrkB signaling as a mediator of brain regeneration following a stab injury in the adult zebra sh brain. Since BDNF has been implicated in a plethora of physiological processes, we hypothesized that these processes are affected in the injured zebra sh brain. In this small study, we examined the indicators of oxidative stress and of apoptosis using biochemical assays, RT-PCR and IHC to re ect upon the impact of stab injury on oxidative stress levels and apoptosis in the injured adult zeba sh brain. Our results indicate induction of oxidative stress in the injured adult zebra sh brain. Also, apoptosis was induced in the injured brain as indicated by increased protein levels of cleaved caspase3 as well as enhanced mRNA levels of both proapoptotic and anti-apoptotic genes. This knowledge contributes to the overall understanding of adult neurogenesis in the zebra sh model and raises new questions pertaining to the compensatory physiological mechanisms in response to traumatic brain injury in the adult zebra sh brain.