LE3 .A278 2023

2023

Wilson, Brian

Acadia University

Bachelor of Science

Honours

Biology

Biology

Neuronal death can arise from acute injury to the brain, aging, and neurodegenerative diseases such as Alzheimer’s, in part due the activation of the inflammatory response in mammals. Zebrafish (Danio rerio), like other non-mammalian vertebrates, have brief periods of inflammation after brain injury followed by neurogenesis. Relaxin-3 (RLN-3) is a neuropeptide member of the relaxin peptide superfamily. It is highly expressed in both the mammalian and teleost fish brain, and it has conserved anti-inflammatory and anti-fibrotic effects in vertebrates. In this study, traumatic brain injuries (TBI) were created in the telencephalic vesicles of anesthetized zebrafish to study the effect of relaxin-3 on acute inflammation and neuronal regenerative abilities. TBI’s were introduced by inserting a 33G needle through the left nostril and into the telencephalic vesicle. The uninjured vesicle served as a control. Zebrafish were treated with PBS (control), RLN-3 4.00x10-9 M, or RLN-3 4.00x10-11 M solutions in 1L of ambient water. A decrease in mean L-Plastin immunoreactive cells in the RLN-3 treated TBI hemispheres was observed 2 days post-injury when compared to the control treatment group. PCNA immunoreactive cell counts were higher in the zone of injury in RLN-3 treated TBI hemispheres when compared to the undamaged hemispheres. However, no significant differences were observed in typical neurogenic zones around the telencephalon. These results suggest that relaxin-3 suppresses inflammation in response to a traumatic brain injury and may allow for neural regeneration in the location of damage in zebrafish. These data point towards a potential therapeutic value for relaxin-3 in treating neurological diseases in humans through the suppression of inflammation and recruiting nearby glial cells to the damaged area.

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https://scholar.acadiau.ca/islandora/object/theses:4032