Neuroscience Unit

Head of Unit: Prof Laurence RIS

The department of Neuroscience hires a post-doctoral researcher for 1 year starting immediately - expertise in patch-clamp is required

 

We are seeking highly motivated candidates to join us on a running project (2019-2023) on the molecular mechanisms of sensory neurogenesis. We study in particular the nociceptors, the specialized peripheral neurons that detect painful stimuli.

Starting date is flexible / possibility to start in May 2021

Neuroscience lab, University of MONS, BELGIUM

We aim to understand the role and mechanism of action of the Prdm12 gene. Prdm12 encodes an evolutionarily conserved epigenetic regulator of gene expression that has been found mutated in patients that suffer from Congenital Insensitivity to Pain. We expect that the results of our work will help in the development of new strategies for treating pain.

The positions are funded by the Walloon government within the frame of the “Win2wal” program. The research will be performed in the laboratory of Neuroscience (Dr. Laurence Ris) at the University of Mons.

The experiment performed will be whole cell patch-clamp on DRG neurons prepared from WT and conditional KO mice (Prdm12) or overexpression mice. Basal electrophysiological properties, excitability and ionic currents (Na VDCC, Ca TRPV).

Interested candidates should send a letter of motivation describing past research experiences and full CV to:

Laurence Ris (Laurence.RIS@umons.ac.be) together with the name and e-mail address of 2 references.

Selected related publication:

Nagy et al., (2015). The evolutionarily conserved transcription factor PRDM12 controls sensory neuron development and pain perception. Cell Cycle, 14(12), 1799-1808.

Research Projects:

• Neuroscience research scientists currently agree that memory is stored in our brain thanks to synapses adjusting their effectiveness to modify neuronal selectivity. Synapses are junctions which link brain cells into a neuronal network;
  
  
• It is possible to start a durable increase in synaptic effectiveness (during several hours) on 0.5 mm thick brain slices (hippocampus), kept alive artificially. This phenomenon is known as long-term potentiation (abbreviated to LTP). LTP thus constitutes a model of elementary memory which can be studied in vitro. These are the two characteristics that make it fascinating to research;
  
  
• The mechanisms which trigger the release of LTP and keep it in its initial phase (first hour) are well-known. However, mechanisms responsible for its longer-term maintenance (in particular from 1 to 4 hours after its induction) are yet unknown;
  
  
• We are currently focusing on the mechanisms of the more durable phase of the LTP (L-LTP or Late Long-Term Potentiation) 

• We also study neuropathologies inducing alterations in memory formation and in long term synaptic plasticity such as alzheimer's disease, multiple sclerosis, traumatic brain injury and post-traumatic stress disorder.

Collaborations:

• Research Institute for Biosciences: collaborative project to study the impact of neuroinflammation induced by a mechanical stress in novel in vitro models. IBS

• Institute of Neurosciences (IoNS) of UCL: collaborative project on alzheimer's disease. IoNS.html

• Kings College London: collaboration to study the role of CaMKII alpha on synaptic plasticity and memory. Kings College