• E-mail :[email]
  • Phone : 01 53 46 25 92
  • Location : Paris, France
Last update 2011-04-18 21:16:39.836

Serge Picaud PhD in Neuroscience

Course and current status


2001                 Authorization in animal research as principal investigator, University Louis Pasteur, France

2000                 Promoted Director of research ( DR2) at INSERM (France)

1999                 Habilitation, Université Louis Pasteur, Strasbourg, France

1997                 Permanent Research Position (CR1) at INSERM, (France)

1990                 PhD in Neuroscience, University of Aix-Marseille, France.

1984                 Master in pharmacology, major in Neurobiology, University of Paris, France.

1981-1985         Ecole Normale Supérieure de l'Enseignement Technique, major in Biochemistry.




2002-                Principal investigator, Institut de la Vision, INSERM, University Paris VI

                        Pr Sahel, Paris, France

                        Retinal information processing: Pharmacology and pathologies


1995-2002         Researcher, University Louis Pasteur/INSERM EMI 99-18

                        Pr Sahel and Dr Dreyfus, Strasbourg, France

                        Photoreceptor function and neuroprotection.


1991-1995         Postdoc, University of Berkeley,

                        Pr. F. Werblin, Berkeley, California, USA.

                        Glutamate transporters.


1987-1988         Predoc, Max-Planck Institut of Brain Research,          

                        Pr H. Wässle, Francfort, Germany.

                        Lesion and gliosis in the mammalian retina.


1984-1987 et 1988-1991             Graduate student, Laboratory of Neurobiology,

                        Dr N. Franceschini, CNRS, Marseille, France.

                        Dye-induced photosensibilisation of invertebrate neurones in vivo.


1983-1984         Institut of Physical and Chemical Biology,

                        Pr J.P. Henry, CNRS, Paris, France.

                        Research of ionic channels in synaptic vesicles.

Scientific summary

Our aim is to investigate retinal information processing and to determine how the underlyng molecular mechanisms can be involved in pathology and/or neuroprotection. We also model retinal information processing to evaluate how to stimulate the retina of blind patients with retinal prostheses or optogenetic tools in order to restore some useful vision.

After having demonstrated how the glutamate transporter controls synaptic release at both the photoreceptor and the bipolar cell terminals, we have investigated the role of inhibitory neurotransmitters at the photoreceptor terminals. We showed that cone photoreceptors express active ionotropic GABA and glycine receptors, and that horizontal cells can synthesize and release GABA at the photoreceptor terminals. To investigate if GABA is implicated in retinal pathologies, we have examined the retinal toxicity of the anti-epileptic drug, vigabatrin. Indeed, this drug is an inhibitor of the GABA-transminase, which increases by 5 fold the retinal GABA. After describing the vigabatrin-induced lesions (cone damage, glial reaction, rod and their bipolar cell plasticity, …), we discovered that vigabatrin triggers a phototoxicity due to a depletion in taurine, an anti-oxidant sharing many common features with GABA. These results have clinical relevance because the plasma taurine of vigabatrin-treated patients is also greatly diminished. In another studies, we demonstrated that an excessive activation of channels activated by cyclic GMP can lead to photoreceptor degeneration.

Considering strategies to restore vision in blind patients, we have first characterized the activity in the residual retina following the photoreceptor loss. Then, we investigated a pharmacological approach to prevent the continuous degeneration of this residual retina. The neuroprotective molecule discovered in this program was also efficient on models of glaucoma. Then, we have designed retinal prostheses with 3D structures, which are evaluated on blind animals. In parallel, we collaborated with Dr Roska to evaluate the use of halorhodopsin, a bacterial protein, to restore vision by gene therapy directed toward cone photoreceptors having lost their photosensitivity.

All these studies were possible thanks to the development of a number of cell and tissue models such as pure cone photoreceptors or retinal explants of human post-mortem retina. Our continuum of technique to assess retinal cell activity can provide single cell recording (patch clamp technique), network recording (multielectrode array) or in vivo tissue recording (electroretinogram). The development of imaging tools is enhancing further our ability to characterize the animal models of retinal pathologies.

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