The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Click here to participate in the public defence
Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Digital Trial Lecture – time and place
Adjudication committee
- First opponent: Professor Antje Grosche, Ludwig-Maximilians-Universität München
- Second opponent: Associate Professor Hakima Moukhles, University of British Columbia
- Third member and chair of the evaluation committee: Associate Professor Torkel Hafting, University of Oslo
Chair of the Defence
Associate Professor Andreas Lossius, University of Oslo
Principal Supervisor
Professor Mahmood Reza Amiry-Moghaddam, Institute of Basic Medical Sciences, University of Oslo
Summary
Glial cells, astrocytes and Müller glia, are involved in homeostatic functions in the CNS. Emanating from these cells are fine processes that interact with vasculature to form ‘glio-vascular’ interface. At this interface, the fine processes enwrap the vasculature and are called endfeet. At this site, K+ channel Kir4.1 and water channel aquaporin-4 (AQP4) are highly expressed in a polarized manner and are involved in buffering K+ and water, respectively. In several pathologies, this polarized distribution is lost suggesting an underlying mechanism that influence the polarity. In this thesis, Shreyas has explored the molecular mechanisms that are responsible for Kir4.1 and AQP4 polarity by use of novel transgenic mouse model. Evidence is provided that β1-syntrophin is involved in tethering Kir4.1 to the endfeet and that both α1- and β1-syntrophin are involved in polarized distribution of AQP4 in retina. Interestingly, β1-syntrophin plays no role in polarized distribution of AQP4 in the brain. These novel insights help us understand the basic physiology and provide future directions in search of causes and potential treatment strategies for diseases affecting the retina and brain.
Additional information
Contact the research support staff.