Stephane Peineau
  • E-mail :[email]
  • Phone : (+33) 03 22 82 79 32
  • Location : Amiens, France
Last update 2017-05-12 12:44:19.851

Stephane Peineau PhD, HDR, Neurosciences, Electrophysiologist

Course and current status

Present Appointment

Researcher; Chair of Excellence "Synaptic Plasticity", GRAP ERI24 , Université de Picardie Jules Verne, Amiens, France

and

Senior Research Associate; Graham Collingridge's Team, University of Bristol, Bristol, UK

 

Previous Appointment

  • 2007-2017: Senior Resarch Associate; Graham Collingridge's Team, University of Bristol, Bristol, UK and UMR1141, Hôpital Robert Debré, Paris , France
  • 2005 - 2006: Research Associate; Graham collingridge's team, University of Bristol, Bristol, UK
  • 2004 – 2005: Research Assistant; Graham Collingridge’s team, University of Bristol, Bristol, UK
  • 2003 – 2004: Postdoctoral Fellow; Graham Collingridge’s team, University of Bristol, Bristol, UK

 

 Academic Qualifications

  • 2016: Habilitation to Conduct Research - University of Paris 7 (Paris, France)
  • 1998-2002: PhD in Neurosciences - University of Paris VI (PhD School: Brain, Cognition, Behaviour), France - Laboratory: INSERM U549 (Paris)
  • 1997-1998: DEA (Diplôme d’Etudes Approfondies) in Neurosciences - University of Paris VI (equivalent of a Master 2, France)
  • 1996-1997: Maîtrise of Cellular Biology and Animal Physiology - University of Tours (equivalent of a Master 1, France)
  • 1995-1996: Licence of Cellular Biology and Animal Physiology - University of Tours (equivalent of a Licence 3, France)
  • 1994-1995: DEUG (Diplôme d’Etudes Universitaires Générales) Biologie II - University of Tours (equivalent of a Licence 2, France)
  • 1993-1994: DEUG (Diplôme d’Etudes Universitaires Générales) Biologie I - University of Tours (equivalent of a Licence 1, France)

Scientific summary

My research works focus mainly on the deciphering of the cellular mechanisms associated with excitatory synaptic transmission inhibition within the brain, especially those involved during  i) long term synaptic plasticity (Long term Depression), ii) neuroinflammation, iii) alcohol consumption (binge Drinking) or iv) neuropeptide release.

Long Term Depression (LTD) is a family of synaptic plasticity mechanisms that can be triggered by the synaptic or pharmacological activation of glutamate receptors, in particular NMDARs and mGluRs, or other neurotransmitter receptors. LTD is expressed by a long lasting decrease in the efficiency of synaptic transmission, in particular that mediated by the synaptic activation of AMPARs, and may involve presynaptic and postsynaptic mechanisms. Complex signalling cascades, involving Ca2+ sensors, protein-protein binding/unbinding, protein kinases and phosphatases, proteases and other signalling molecules, link induction to expression of LTD. We have identified two new signalling pathways crucial for LTD induction: the first one involves Glycogen Synthase Kinase 3 (GSK3) and Protein Phosphatase 1 (PP1), the second one involves the "inflammatory signalling cascade" Janus Kinase 2 (JAK2) / signal transducer and activator of transcription 3 (STAT3).

Neuropeptides and molecules released during neuroinflammation, like cytokines, interacting with neuronal function have turned out to be a major regulatory mechanism in the control of neuronal excitability and neuronal network activity leading them to play an important role on neuroendocrine, motor and cognitive functions. 

By studying somatostatin inhibition of excitatory transmission, we have shown that somatostatin induced inhibition of AMPAR currents requires a concomitant activation of sst2 receptors with either NMDARs and/or mGluRs. This modulation depends on changes in intracellular calcium concentration induced by calcium flux through NMDARs or calcium release from intracellular stores following mGluRs activation. Sst2 receptors are subject to an intense trafficking and this is believed to interfere with the capacity of somatostatin to modulate excitatory signalling.

Our last works show a complex relationship between the glutamatergic system and the immune system. On one side, immune system is dependant of the glutamatergic system and on the other side, the neuroinflammation is a powerfull modulator of glutamatergic synaptic plasticity by directly interacting at the level of the synaptic plasticity intraneuronal signalling pathways.

Interestingly, binge drinking leads to LTD suppression and is associated with a neuroinflammatory pattern. We are now investigating the links between Alcohol, neurinflammation and synaptic plasticity alterations.

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