Melatonin Induces per1a Expression in Zebrafish Brain
DOI:
https://doi.org/10.36877/pmmb.a0000455Abstract
In vertebrates, the circadian mechanism regulates many physiological and behavioral activities. The major key output of the circadian clock is the secretion of melatonin in the pineal gland. Melatonin secretion remains low during the daytime and increases significantly at night. The rise and fall of melatonin level is a key factor that conveys rhythmic information to the organism to carry out daily and annual physiological rhythms. It also affects the rhythmic oscillation of clock genes in the suprachiasmatic nucleus (SCN) as well as in peripheral tissues. In this study, we have shown that zebrafish brain rhythmically expresses per1a and cry1a in different photoperiodic regimes: light-dark cycle (LD) and continuous light (LL). We have also demonstrated that an acute injection of melatonin in the middle of the subjective day induces per1a expression in zebrafish brain. Furthermore, we have also shown that an acute injection of melatonin affects circadian regulation of locomotor activity in zebrafish under LD conditions. These results provide insight into understanding the underlying mechanism of melatonin in regulation of clock genes and locomotor activity in zebrafish.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2024 Cher Ryn Lim, Zhen Xuen Brandon Low, Tomoko Sogo, Yatinesh Kumari
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
Author(s) shall retain the copyright of their work and grant the Journal/Publisher right for the first publication with the work simultaneously licensed under:
Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). This license allows for the copying, distribution and transmission of the work, provided the correct attribution of the original creator is stated. Adaptation and remixing are also permitted.
Â
This broad license intends to facilitate free access to, as well as the unrestricted reuse of, original works of all types for non-commercial purposes.
The author(s) permits HH Publisher to publish this article that has not been submitted elsewhere.