Líffræðifélag Íslands - biologia.is
Líffræðiráðstefnan 2017

Erindi/veggspjald / Talk/poster E65

Sleep in VMAT2 Mutant Zebrafish

Höfundar / Authors: Pablo Botella (3), Valerie H. Maier (4), Haraldur Þorsteinsson (1), Karl Ægir Karlsson (1,2)

Starfsvettvangur / Affiliations: 1. 3Z Pharmaceuticals, Reykjavik Iceland, 2. School of Science and Engineering, Reykjavik University, Reykjavik Iceland, 3. Universidad Autonoma de Madrid, Madrid, Spain, 4. Biomedical Center, University of Iceland, Reykjavik, Iceland.

Kynnir / Presenter: Pablo Botella Lucena

Abstract Recent evidence indicates that polymorphisms in the gene encoding VMAT2 monoamine vesicle transporter play a role in Parkinson´s disease (PD). Mutations of this gene lead to failed import of monoamines into vesicles, one of the hallmarks of PD. The ensuing lack of dopamine signalling has raised the hopes that studying VMAT2 function in mutant animal models represents a putative model of PD. In the current study we use zebrafish to assess behavioural phenotypes affected in PD, motor patterns, sleep and anxiety, in a VMAT2 mutant line. First, a motor assay revealed that homozygous VMAT2 mutants have a lower overall swim velocity compared to wild-type or heterozygous larvae. Second, they display higher levels of thigmotaxis (a well-known correlate of anxiety in fish), and third, they have higher levels of sleep with fewer awakenings during the night. We conclude that VMAT2 mutant fish share motor impairments and increased anxiety with human sufferers of Parkinson´s. Sleep patterns, however, differ between the zebrafish model and humans, with homozygous mutants sleeping more rather than less.