Scientific Registration

Scientific Registration at the GRAND HOTEL DES THERMES , Brides les Bains, France 

Saturday, March 7 : 17:00 – 19:30 and Sunday, March 8 : 16:30 – 19:30 

Corinne Kanakis, Congress Registration Desk 


Opening of the 35th EWCBR & EBBS Winter Conference

Monday March 9th - 8:30-8:45

Chairman : Walter Zieglgänsberger 

Session 1

Monday March 9th - 8:45-10:45

Consequences and mechanisms of neuroimmune interactions 

Chair: Mats Lekander, Karolinska Institute/Stockholm University, Sweden 


The importance of neuroimmune interactions for pain and the chronicity of pain in animal models is becoming increasingly clear. In humans, the impact on brain function from inflammation starts to be delineated, including mechanisms behind subjectively oriented symptoms that come as consequences of neuroimmune interaction during activation of innate immunity. The session will address mechanisms for pain sensitivity and resolution of pain, and how peripheral inflammation regulates human brain function. The question whether behavioral changes in subjectively oriented diseases are reflected in measures of low-grade inflammation will also be addressed.

Niels Eijkelkamp, UMC Utrecht, Netherlands: A novel biologic agent for targeting neuroinflammation to treat chronic pain

Harald Engler, University Hospital Essen, Germany: Inflamed moods: fingerprints of peripheral inflammation in the human brain

Mats Lekander, Karolinska Institute/Stockholm University, Sweden: From inflammation to behavior and back again: brain regulation of immunity or the other way around? 

Session 2

Monday March 9th – 16:30 – 19:30 

Non-invasive brain stimulation


Christoph S. Herrmann (Oldenburg, Germany) 


Non-invasive brain stimulation (NIBS) serves two important goals. Firstly, NIBS allows to modulate brain activity and thus is an important tool in basic neuroscience. By stimulating a brain region via NIBS, a causal role of that region for a certain cognitive or motor function can be demonstrated. Secondly, NIBS can be used to induce plastic changes in neural circuitry potentially leading to therapeutic applications in many neurological and psychiatric disorders. The speakers of the intended symposium will describe the development of this exciting field and its current state of the art. Risto Ilmoniemi, the founder of the company Nexstim, will give a presentation on the state of the art in transcranial magnetic stimulation (TMS). Gregor Thut will demonstrate how repetitive protocols of TMS can be used to entrain brain oscillations and, in turn, to modulate cognition. Walter Paulus will demonstrate how another type of NIBS called transcranial direct current stimulation (tDCS) interferes with brain activity and motor function. Christoph Herrmann will introduce transcranial alternating current stimulation (tACS) that is able to modify brain oscillations as demonstrated with electroencephalography (EEG). Finally, Nathan Weisz will present new data on how the neural effects of tACS can be monitored with magnetoencephalography (MEG). 


Risto Ilmoniemi, Aalto University, Helsinki: Transcranial magnetic stimulation 

Gregor Thut, University of Glasgow: Repetitive transcranial magnetic stimulation 

Walter Paulus, Göttingen University Hospital: Transcranial direct current stimulation 

Christoph S. Herrmann, European Medical School Oldenburg: Transcranial alternating current stimulation in EEG 

Nathan Weisz, University of Trento: Transcranial alternating current stimulation in MEG  

Session 3

Tuesday March 10th – 8:30 – 10:30 

Gap Junctions in a therapeutic context for brain disease 

Co-Chairs: Christian Naus and Marc Mesnil 

Cells within the CNS communicate at many levels involving processes ranging from neuronal synaptic interactions, astrocyte networks, gliovascular regulation, inflammatory microglia and myelinating oligodendrocytes. One typical feature of glial cells is their high expression level of gap junction proteins, named connexins, thus the membrane channels they form have been shown to contribute at many levels of brain function. While gap junction channels provide the basis for a unique direct cell-to-cell communication, connexin hemichannels allow the exchange between the cytoplasm and the extracellular medium, thus supporting autocrine and paracrine communication, as well as uptake and release of metabolites. More recently, another family of gap junction proteins has been identified, termed pannexins; these proteins share similar membrane topology but no sequence homology with connexins. They also form hexameric membrane channels with a pharmacology somewhat overlapping with connexin hemichannels. In this workshop, we discuss how gap junctions, hemichannels and pannexin channels may function in brain health and disease. A common theme for each talk will be potential therapeutic applications targeting gap junctions in the CNS. 

Marc Mesnil, University of Poitiers, France: Gap junctions in growth control and invasion in glioma: a proteomic approach

Luc Leybaert, University of Gent, Belgium: Radiation bystander effects mediated by brain endothelial gap junctions

Steffany Bennett, University of Ottawa, Canada: Pharmacological modulation of connexin function to promote oligodendrocyte survival and direct oligodendrocyte replacement in multiple sclerosis

C. Naus, University of British Columbia, Vancouver, Canada: Targeting gap junction hemichannels in stroke

Session 4

Tuesday March 10th – 16:30 – 19:30 

External factors influence on vulnerability to addiction 

Christelle BAUNEZ, CNRS & AMU UMR7289, Marseille, France 

How some individuals can maintain a recreative consumption of substances of abuse and others precipitate into addiction remains an unsolved question. Vulnerability to addiction seems however to be under the influence of various factors that have been studied. The present symposium aims at highlighting some of these factors that could play either a protective or an aggravating role n the process of addiction. Prof. M. Naassila (INSERM Amiens, France) will present how exposure to alcohol at the adolescent stage can influence vulnerability to alcoholism at the adult stage. In contrast, Dr. M. Cador (CNRS Bordeaux, France) will present how sucrose consumption at the adolescence can have a protective effect on alcohol consumption at the adult stage. The environmental context can also play a critical role in the process of addiction and this will be reviewed by Prof. A. Badiani (Univ La Sapienza, Rome, Italy & Univ Sussex, Brighton, UK) who will describe how resident rats show a preference for consumption of heroin over cocaine, while non resident rats prefer cocaine over heroin. Finally, Dr. C. Baunez (CNRS Marseille, France) will focus on the influence of proximal social factors, such as the presence of a peer, on cocaine intake and will provide some neurobiological basis for this influence. 

M. Naassila, Université de Picardie Jules Verne, Amiens: Early onset alcool consumption on the vulnerability towards alcoholism 

M. Cador, Université Bordeaux Segalen: Adolescent sucrose consumption on future addictive behavior towards alcohol 

A Badiani, Sapienza University of Rome: Opposite influences of environmental context on cocaine and heroin reward 

Elodie Giorla, Institut de Neurosciences de la Timone Aix Marseille Université: Role of the STN on the influence of proximal social factors on cocaine consumption 

Session 5

Wednesday March 11th – 8:30 – 10:30 

Therapeutic applications for animal venom toxins 

Chair: Michel de Waard (Institut des Neurosciences, Grenoble, France) 

Abstract : 

Maurocalcine is an animal peptide originally isolated from the Tunisian scorpion Scorpio maurus palmatus. It belongs to the toxin family that folds according to an inhibitor cystine knot, it possesses 3 disulfilde bridges, and is composed of 33 residues. The toxin is peculiar because of its unusual composition in positively charged residues that create a strong dipole moment. These features favor its penetration into cells. Once inside, it then binds onto an intracellular ion channel, the ryanodine receptor that it activates to promote calcium release from the endoplasmic reticulum. Of interest, the peptide shares restricted sequence homology with the cell surface voltage-gated dihydropyridine receptor and binds similarly than this channel onto the ryanodine receptor thereby becoming an exquisite molecular tool to understand how excitation contraction works in skeletal muscles. 

Besides its unique pharmacological properties, it was soon realized that the peptide is also an excellent vector for the delivery of therapeutic drugs, imaging agents or nanoparticles. This peptide was then derived in multiple ways to restrict the pharmacological activation of the ryanodine receptor but preserve its cell penetration capacity. Several new vectors were designed and many applications developed. We will present one application which consists in fighting chemo-resistance of tumor cells. Due to its ability to remain confined within cells once it gets inside them, coupling anti-tumor agents to maurocalcine-derived vectors appears as an excellent technical solution to avoid drug efflux by the Multidrug Resistance Protein. 

Nicolas Gilles, Institut de Biologie et de Technologie de Saclay, France: Mambaquaretin, a green mamba toxin as a new therapeutic agent for polycystic kydney diseases 

Session 6

Wednesday March 11th – 16:30 – 19:30 


Chairs: William Rostène, Annabelle Réaux Le Goazigo 


First discovered in the late 1980s, chemokines (chemoattractant cytokines) are a family of low-molecular-weight proteins. Chemokines can be induced during an immune response to recruit cells of the immune system to a site of infection. Immune cells include bone-marrow mononuclear progenitors, blood monocytes, macrophages and microglial cells. Several pathologies such as age related macular degeneration (AMD), spinal cord injury and chronic pain are characterized by immune cell infiltration orchestrated by chemokines. More recently, it has been also established that chemokines also play a crucial role in the central nervous system by exerting deleting or neuroprotective effects, modulating neurotoxicity through for instance CX3CL1/CX3CR1 signaling. Furthermore, chemokines are able to interact with opioid system to modulate opioid analgesia. Thus, this session will cover various aspects of the neuro-immune interactions, orchestrated by immune cells and chemokines, which occur during various CNS pathologies and will propose novel strategies towards these pathologies. 



Therapeutic department, Institut de la Vision UMR S 968 Inserm/ UPMC/ CNRS 7210 Paris Mail 

Neuronal toxicity of Cx3cr1-deficient mononuclear phagocytes during subretinal inflammation 

Shulong Hu, Bertrand Calippe, Sophie Lavalette, Florian Sennlaub, Xavier Guillonneau. 

Age-related Macular Degeneration (AMD) is the leading cause of irreversible blindness in the developed world. Subretinal mononuclear phagocytes (MPs) accumulate in the vicinity of the atrophic lesion of AMD patients. We have recently shown that subretinal MPs that originate from the blood circulation and accumulate in the subretinal space are particularly detrimental in animal models of subretinal inflammation. Defects in the CX3CR1/CX3CL1 axis are associated in animals with cardinal features of AMD including photoreceptor loss. Here we show that Cx3cr1-deficient MP overexpress the surface receptor P2X7 that stimulates IL-1β maturation and secretion. P2X7 and IL-1β inhibition efficiently blunted photoreceptor apoptosis of Cx3cr1-deficient MP in a monocyte/retina co-culture system and P2X7 inhibition significantly diminished photoreceptor cell death in light-induced subretinal inflammation in vivo. Our results provide new rationals to protect retina from damaging age-dependent subretinal inflammation. 


Department of Physiology and Pharmacology, Istituto Pasteur Fondazione Cenci Bolognetti, Sapienza University of Rome Rome, Italy ; Istituto di Ricovero e Cura a Carattere Scientifico Neuromed, Istituto Neurologico Mediterraneo Pozzilli, Italy. 

Mail : 

The chemokine CX3CL1 and its receptor CX3CR1 are constitutively expressed in the nervous system. Recent exciting evidence indicate that CX3CL1-mediated microglia-neuron interaction modulates basic physiological activities during development, adulthood and aging, including: synaptic pruning; promoting survival of neurons and neural precursors; modulating synaptic transmission and plasticity; enhancing synapse and network maturation and facilitating the establishment of neuropathic pain circuits. Beyond playing such fascinating roles in physiological conditions, CX3CL1 signaling has been implicated in different neuropathologies. Thus, CX3CL1 drives interplay between neurons, microglia and astrocytes to counteract pMCAO and excitotoxic neuronal death. 



Therapeutic department, Institut de la Vision UMR S 968 Inserm/ UPMC/ CNRS 7210 Paris Mail: 

Chemokines as modulators of opioid functions in pain pathways 

Chemokines and opioids play major roles in regulating immune, inflammatory and neuronal responses in peripheral and central pain pathways. Recent studies provide insights into the functional interactions between chemokine and opioid receptors and their role in pain modulation. We recently evaluated whether Src family-kinases (SFK)-linked mechanisms induced by CXCR4 contributed to the loss of acute morphine analgesia and could represent a new physiological anti-opioid signaling pathway. We reported that CXCR4, the CXCL12 receptor, was detected in MOR-and DOR-immunoreactive neurons in the DRG and spinal cord. In vivo, we showed that an intrathecal administration of CXCL12 significantly decreased the subcutaneous morphine analgesia by heterologous desensitization of opioid receptors. Conversely, pretreatment with a CXCR4 antagonist enhanced morphine analgesia. Similar effects were obtained after an intrathecal injection of a specific SFK inhibitor, PP2. Furthermore, PP2 abrogated CXCL12-induced decrease in morphine analgesia by suppressing SFK activation in the spinal cord. In conclusion, our data highlight that CXCL12-induced loss of acute morphine analgesia is linked to Src family kinases activation. Although chemokines are present at relatively low concentration in the brain, particularly in neurons, they seem to have important functions. An understanding of their function and cross talk with opioid receptor functions could shed light on the coordination and fine-tuning of several types of neurobiological responses, including acute pain and chronic pain states. 


Groupe Interdisciplinaire de Génoprotéomique appliquée (GIGA), Neurosciences Unit, University of Liège, Avenue de l'Hopital 1 - B36, Liège, 4000, Belgium - Mail : 

Immunomodulatory properties of adult mesenchymal and neural crest stem cells : Relevance in spinal cord injury and repair. 

Spinal cord injury (SCI) treatment represents a critical issue in clinical research and patient care. Stem cell-based replacement therapies have already been proposed worldwide, especially studying stem cells from the adult bone marrow stroma. Previous studies focusing on those cells did not specifically consider their intrinsic embryonic heterogeneity, thus intermingling different stem cells subpopulations to treat experimental SCI or even injured patients. We decided to compare adult bone marrow neural crest-derived stem cells (NCSC) and mesenchymal stem cells (MSC), and highlight which of their specific properties could be relevant in therapeutic perspectives. In that purpose, we compared NCSC and MSC isolated from adult mouse bone marrow. We know that adult stem cells mainly act through paracrine secretion, and have immunomodulatory properties. It is well accepted that the immune response and subsequent inflammatory reaction are of significant importance in regulating the damage/repair balance after SCI. Indeed, recent data show that immune cells such as macrophages or neutrophils are required for promoting functional recovery after spinal cord trauma. Therefore, fine-tuning of the inflammatory reaction through cytokines and chemokines signaling needs to be investigated. Altogether, studying stem cell-based immunomodulation should help to improve and optimize cell-based therapies parameters and/or to define precise and efficient pharmacological treatments for SCI patients. 


Session 7/1

Thursday March 12th – 08:30 – 10:30 (Oral, Morning)

Vision loss: dysfunction, plasticity, restoration and rehabilitation

Chair: B. Sabel

Waleszczyk Wioletta, Poland: Changes in neuronal activity in the visual cortex and subcortical structures of the visual system following posterior cortical stroke

Liu, Hongjun, USA: Regeneration of retinal neurons and glia by Lgr5+ amacrine cells in adult mice

Vaucher, Elvire, Canada: Effect of enhancement of the cholinergic transmission on perceptual-cognitive training of healthy young adults

Heutink, Joost, Netherlands: The DiaNAH test battery: a 30-minute computerized screening for perceptual disorders

Kurysheva, Natalia, Russia: New technologies in glaucoma diagnosis and management 

Session 7/2

Thursday March 12th – 16:30 – 19:30 (Oral, afternoon)

Vision loss: dysfunction, plasticity, restoration and rehabilitation

Chair: B. Sabel

Gera de Haan, Netherlands: Specificity of the effects of compensatory scanning training for patients with homonymous visual field defects

Collignon, Olivier, Italy: Impact of sight deprivation and restoration on the functional organization and connectivity of the occipital cortex

Elisabetta Làdavas, Italy: Multisensory stimulation in hemianopic patients boosts orienting responses to the hemianopic field and reduce attentional resources to the intact field

Bernhard Sabel, Germany: Vision restoration and brain functional connectivity network reorganization

Poster session:



  Restoration of vision can also improve sound localization: cross-sensory calibration? 



  Visual BOLD response in late-blind subjects with Argus II retinal prosthesis 

 Tinelli, F


  Reorganization of the visual pathways after early-age tumor surgery: the contribution of functional     magnetic resonance imaging and fiber tractography   

Session 8

Thursday March 12th – 16:30 – 19:30 

Regulatory processes in brain-body interaction 

Chair: John Axelsson, Karolinska Institute/Stockholm University, Sweden 


With new techniques to study human brain function, even subtle processes as expectation and learning in relation to bodily processes can be studied and integrated with knowledge on peripheral processes, including more automatically processes such as behavioral conditioning. This forms an increasingly coherent picture of how bodily processes can be regulated, with bearings on e.g. placebo or regulation of emotional processes in psychiatric disorders. Successful regulation is in turn dependent on restitution and biological rhythms in a way that is relevant both for everyday functioning and severity of psychiatric symptoms. In the session, recent knowledge concerning mechanisms and consequences of both central and peripheral regulatory processes will be highlighted.

Sigrid Elsenbruch, University of Duisburg-Essen, Germany: Hoping for the best but expecting the worst: The role of expectation and learning in visceral pain processing

Manfred Schedlowski, University of Duisburg-Essen, Germany: Teach the T cells: How learning can shape immunity

Julie Lasselin, Karolinska Institutet Sweden: Low-grade inflammation and fatigue, sleepiness and sleep

John Axelsson, Karolinska Institutet Sweden: Do we adapt or maladapt to sleep loss?

Predrag Petrovic, Karolinska Institutet, Sweden: Brain regulation of emotional processes

Session 9

Friday March 13th – 08:30 – 10:30 

Does epilepsy re-program the brain? 

Chair : Claude Wasterlain 


This session focuses on how epilepsy changes the brain in many ways, ranging from plasticity of the neurovascular unit to activity-associated neuronal injury and to activity-associated changes in expression of fundamental biological programs. Christophe Bernard will discuss the re-programming of the circadian clock in epilepsy, a novel concept supported by considerable evidence. Denny Fujikawa will review the role of neuronal firing in drug-induced neuronal injury, and its relevance to epilepsy. Andre Obenaus will discuss the role of vascular factorts in the development of post-traumatic epilepsy. Claude Wasterlain will re-visit the concept of critical periods of brain development, and show that vulnerability to seizure-induced neuronal injury can start much earlier in life than was previously thought, and modify developmental programs in specific neuronal populations. 


Christophe Bernard, France: The circadian hippocampus and its reprogramming in epilepsy 

Denny Fujikawa, USA: Electrographic seizure discharges and methamphetamine-induced neuronal necrosis

Andre Obenaus, USA  Do vascular alterations contribute to post-traumatic epilepsy?

Claude Wasterlain, USA: Seizures, neuronal injury, and critical periods of brain development

Stefania Zappettini, Marseille: Enhanced sensitivity to seizures after caffeine exposure during pregnancy. A role for A2A receptors.

Session 10

Friday March 13th – 16:30 – 19:30 

New diagnostic trends in sever epilepsy 


Olaf B. Paulson, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark 


Electroencephalography (EEG) is the classical method for investigating epilepsy. Newer in the investigation of epilepsy are fMRI, magnetoencephalography (MEG) and molecular imaging. Stefan Posse will discuss the use of high speed fMRI with time of repetition below .5 sec compared to the classical value of 2 sec yielding a much improved temporal resolution. The short time of repetition has special interest when combining fMRI with EEG. Sándor Beniczky will report on source localisation in epilepsy using EEG and MEG and compare the two methods. Olaf Paulson will report on a newly started project combining fMRI with simultaneous EEG with possibilities of 256 simultaneous EEG channels. Lars Pinborg will report on the use of SPECT and PET in focal epilepsy. 


Stefan Posse, University of New Mexico, Albuquerque, USA: Functional connectivity dynamics in epilepsy using high-speed fMRI 

Sándor Beniczky, Dianalund & Aarhus, Denmark: Electromagnetic source imaging 

Olaf B. Paulson, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark: Combining fMRI and EEG 

Lars Pinborg, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark: Neurochemical changes in epilepsy demonstrated using molecular imaging