Effects of nicotine-colchicine induction in neurodegenerative behavioral signs in a zebrafish (danio rerio) model

• Main Authors: Borromeo, Sean S., Cortez, Mark G., Macasaet, Linus C., Rivera, Ysabel T.
• Format: text
• Language: English
• Published: Animo Repository 2024
• Subjects: Zebra danio; Colchicine; Nicotine; Nervous system—Degeneration; Biology
• Online Access: https://animorepository.dlsu.edu.ph/etdb_bio/80
• Institution: De La Salle University

Neurodegenerative diseases (ND) are characterized by several core mechanisms linked to the gradual impairment and death of neurons, including oxidative stress and neuroinflammation. Zebrafish (Danio rerio) have emerged as a valuable model for studying neurodegeneration-like symptoms due to their genetic similarities to humans and well-characterized nervous system. This study aimed to investigate the effects of colchicine and nicotine on zebrafish behavior to evaluate their potential synergistic and sequential interactions in a neurodegenerative model. Specifically, the pre-test trial sought to determine a viable concentration of colchicine that would minimize mortality, allowing for subsequent behavioral experimentation. The pre-test trials involved two different concentrations of colchicine. The first trial, using 25 µg/mL, resulted in a high mortality rate of 53.33% within 24 hours. A subsequent trial with a lower concentration of 5 µg/mL demonstrated no mortality over a 72-hour period, establishing this dosage as suitable for the actual experiment. The actual experimentation included five groups with 15 samples each: Control, Nicotine group, Colchicine group, Nicotine followed by Colchicine, and Colchicine followed by Nicotine. Behavioral tests were conducted using Noldus EthoVision XT 17 software to analyze variables such as velocity, distance moved, acceleration, meander, and body contact of the groups. Zebrafish exposed to 5 µg/mL colchicine successfully exhibited neurodegeneration-like symptoms without mortality, indicated by decreased velocity and distance moved compared to control (p < 0.05). The group exposed to nicotine alone showed increased anxiety-related behaviors. Nicotine's potential disruption of the blood-brain barrier facilitated colchicine's neurotoxic impact, particularly, group exposed to nicotine-colchicine, leading to significant behavioral impairments such as increased disorientation, decreased velocity, and decreased distance moved (p < 0.05). Sequential exposure to nicotine followed by colchicine and vice versa resulted in compounded anxiolytic effects. The group exposed to colchicine-nicotine exhibited significant motor impairments, evidenced by reduced distance moved and velocity, highlighting the potentiation of colchicine’s neurotoxic effects by prior nicotine exposure (p < 0.05).