Digital Public Defence: Daniel Lawer Egbenya
MSc. Daniel Lawer Egbenya at Institute of Basic Medical Sciences will be defending the thesis “Changes in plasticity-related proteins in hippocampal synapses in a rat model of chronic temporal lobe epilepsy” for the degree of PhD (Philosophiae Doctor).
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.
Digital Trial Lecture – time and place
- First opponent: Professor Christophe Mulle, Université de Bordeaux
- Second opponent: Associate professor Cecilie Morland, University of Oslo
- Third member and chair of the evaluation committee: Professor Ulrik Fredrik Malt, University of Oslo
Chair of the Defence
Professor Mahmood Reza Amiry-Moghaddam, University of Oslo
Professor Svend Davanger, University of Oslo
Hyperexcitability is a pivotal factor in various neurological diseases. Caused by excessive stimulation of glutamate receptors in the brain, it results in pathologically increased intracellular Ca2+-concentrations leading to acute, pathological molecular changes. Little is known, however, about any possible chronic changes in synaptic plasticity-related proteins in surviving glutamatergic synapses after cerebral insult. To examine these possible long-term changes, three groups of proteins were studied: synaptotagmin 1, a presynaptic calcium sensor that functions in SNARE-mediated vesicular neurotransmitter exocytosis; AMPA receptors, which are responsible for mediating the postsynaptic effect of presynaptic glutamate release; and Arc and BDNF, synaptic plasticity-related immediate early gene products. A kainic acid-based rat model of chronic temporal lobe epilepsy (TLE) was used. We found significant reductions in the concentration of synaptotagmin 1, the AMPA receptor subunits GluA1 and GluA2, and Arc in hippocampal synaptosomes following chronic TLE. An increase was found in BDNF concentration as well. To determine the precise subcellular localisation in which these changes occurred, we performed quantitative postembedding immunogold electron microscopy. Significant reductions of synaptotagmin 1, GluA1, GluA2 and Arc in Schaffer collateral synapses in the hippocampal CA1 area were found. Significant increase in BDNF was found, predominantly, in CA3 presynaptic terminals. Overall, these suggest that there are long-term changes in plasticity-related proteins in surviving glutamatergic synapses in a rat model of chronic TLE. These changes may possibly be neuroprotective by decreasing both pre- and post-synaptic calcium sensitivity following chronic TLE, or they may be destructive by contributing to further aggravate the excitotoxic vulnerability of the neurons. Further research is needed to ascertain whether these changes in synaptic plasticity-related proteins may also influence cognition during chronic TLE.
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