Abstract
Recent findings suggest a significant role of the brain-derived neurotrophic factor (BDNF) as a mediator of brain regeneration following a stab injury in zebrafish. Since BDNF has been implicated in many physiological processes, we hypothesized that these processes are affected by brain injury in zebrafish. Hence, we examined the impact of stab injury on oxidative stress and apoptosis in the adult zebrafish brain. Stab wound injury (SWI) was induced in the right telencephalic hemisphere of the adult zebrafish brain and examined at different time points. The biochemical variables of oxidative stress insult and transcript levels of antioxidant genes were assessed to reflect upon the oxidative stress levels in the brain. Immunohistochemistry was performed to detect the levels of early apoptotic marker protein cleaved caspase-3, and the transcript levels of pro-apoptotic and anti-apoptotic genes were examined to determine the effect of SWI on apoptosis. The activity of antioxidant enzymes, the level of lipid peroxidation (LPO) and reduced glutathione (GSH) were significantly increased in the injured fish brain. SWI also enhanced the expression of cleaved caspase-3 protein and apoptosis-related gene transcripts. Our results indicate induction of oxidative stress and apoptosis in the telencephalon of adult zebrafish brain by SWI. These findings contribute to the overall understanding of the pathophysiology of traumatic brain injury and adult neurogenesis in the zebrafish model and raise new questions about the compensatory physiological mechanisms in response to traumatic brain injury in the adult zebrafish brain.
Highlights
In the past three decades, the teleost zebrafish has emerged as a simple vertebrate model to investigate brain development, normal brain physiology and the mechanisms of neurological diseases
As previously reported (Cacialli et al 2018), the mRNA levels of pcna increased after stab injury in a temporal manner, i.e. it gradually increased over time (Fig. 1a)
This is in contrast to pcna, in which case, the proliferation is maximum around 4DPI. These results indicate that there might be a temporal separation between the activation of the brain derived neurotrophic factor (BDNF)/TrkB signaling pathway and the proliferation response after stab injury
Summary
In the past three decades, the teleost zebrafish has emerged as a simple vertebrate model to investigate brain development, normal brain physiology and the mechanisms of neurological diseases. Both larval and adult zebrafish serve as excellent model organisms for understanding the normal brain functions, complex brain disorders and their genetic and pharmacological modulation. In contrast to adult mammals, which have a relatively poor regenerative ability, adult zebrafish can repair an injury in almost any part of the brain. The reason for this disparity in the brain regenerative ability is not clear. A comprehensive understanding of the cellular and molecular mechanisms orchestrating adult neurogenesis and brain regeneration in zebrafish is desired
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