Zebrafish (ZF) is an incredible animal for the study of neurological disorders. Its behaviour is like higher vertebrate animals, which makes it gainful and robust. Understanding the psychological and biological implications of housing settings for ZFs is very crucial in improving the replicability and dependability of ZF behavioural research. Individual housing triggers depression-like symptoms that suggest that housing conditions have negative effects on ZF and can result in the data discrepancy. Based on various behavioural analyses, we have evaluated that the ZFs kept in isolation and the ZFs kept in herd conditions exhibit different behavioural patterns. Interestingly, normal isolated subjects exhibit similar behavioural patterns as Alzheimer disease (AD)-induced subjects; hence, this can have serious implications on any study concerning behaviour of ZFs. Therefore, we have reported a new behavioural test named “Alarm Test”, which effectively discriminates normal isolated subjects from AD subjects. Alarm Test is observed to be better than other tests used for studying fear and anxiety in ZFs as it uses the indigenous compound released by ZFs during fear and makes use of the same for analysis. This can reduce the involvement of chemicals during behavioural analysis as well as sacrifice of ZFs for collection of alarm substance.
Part of the book: Zebrafish in Biomedical Research
Epilepsy is a noncommunicable disease of the brain that affects people of all ages. The chapter aims to identify protein targets and their mechanism of action behind temporal lobe epilepsy. Differentially expressed proteins in temporal lobe epilepsy (TLE) were used to derive a hypothesis demonstrating routes of protein interactions causing focal seizure and identification of putative target receptor for its treatment. Text mining was done by constructing a Boolean query with keywords such as temporal lobe epilepsy, focal seizures, proteomics, etc., in different scientific search engines. The proteins were further used for creating protein interaction network and analysed for their role in focal epileptic seizure pathway. The most appropriate route for initiation of seizure was observed to be route 3. It describes the dysregulated signal transduction from adenosine A1 receptor (ADORA1) to gamma-aminobutyric acid (GABA) B receptor 1 (GABBR1). This causes electrical imbalance and hyper-excitation of neurons that lead to focal seizure. The study also predicts that YWHAZ (3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta) could be the potential target for preventing focal seizures. The network framed in this study is ideal for studying the cascades of events that may occur during focal seizures in TLE and is useful in drug discovery.
Part of the book: Neurodegenerative Diseases