4.6 Article

Temporal exposure to chronic unpredictable stress induces precocious neurobehavioral deficits by distorting neuromorphology and glutathione biosynthesis in zebrafish brain

期刊

BEHAVIOURAL BRAIN RESEARCH
卷 418, 期 -, 页码 -

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ELSEVIER
DOI: 10.1016/j.bbr.2021.113672

关键词

Chronic unpredictable stress; Neurobehavioral deficits; Oxidative stress; Pyknosis; Chromatin condensation; Zebrafish

资金

  1. Centre for Biotechnology, SOA (Deemed to be University)
  2. UGC start-up research grant
  3. collaborative ICMR extramural research grant

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Zebrafish is a promising animal model for translational research due to its genetic and epidemiological similarities with humans. Chronic unpredictable stress (CUS) can alter zebrafish behavior and brain glutathione biosynthesis, leading to neuromorphological changes. The study suggests that CUS-induced neurobehavioral transformation is associated with oxidative stress and neuromorphological alterations in the zebrafish brain, providing insights for therapeutic interventions.
Modelling of chronic stress conditions in experimental animals and its neuropsychiatric outcomes has been well documented in literature. Zebrafish (Danio rerio) by exhibiting significant genetic and epidemiological similarities with human beings, has now emerged as a promising animal model of translational research. In this line, risk assessment following exposure to chronic unpredictable stress (CUS) towards neurobehavioral response and neuromorphology of sensitive brain region in zebrafish is the prime objective of the present study. With the existing knowledge on CUS in affecting diverse neurobehavioral aspects, we were primarily interested in whether this neurobehavioral transformation is an outcome of altered glutathione biosynthesis in zebrafish. We were also concerned about whether the precocious neurobehavioral transformation has been linked to altered neuromorphology in the periventricular grey zone (PGZ) of the zebrafish brain. Our basic findings showed that CUS itself represented as a universal factor in altering native bottom-dwelling and scototaxis behaviour of zebrafish. Our findings also backing the argument that CUS itself represented a collective stress regimen by altering the brain glutathione biosynthesis in zebrafish. Correspondingly, a temporal transformation in CUS instigated augmentation in neuronal pyknosis and chromatin condensation were observed in PGZ of the zebrafish brain. Collectively, these findings designate that CUS induced temporal neurobehavioral transformation is an outcome of augmented oxidative stress and neuromorphological alteration in the zebrafish brain. However, the underlying mechanism of such neuropathological manifestation associated with CUS might provide novel insight towards the development of prophylactic/therapeutic intervention to counter such co-morbid behavioral alteration.

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