Causal Neuroscience: From Synaptic Plasticity to Adaptive Behavior


June 7 - 14, 2014


Coordinator: Christian Lüscher

University of Geneva, Switzerland



Naoshige Uchida, Harvard University, Boston, USA

Barry Everitt, University of Cambridge, UK

Andreas Lüthi, F. Miescher Institute for Biomedical Research, Basel, Switzerland

Kay Tye, Massachusetts Institute of Technology, Boston, USA

Antonello Bonci, National Institute of Drug Abuse, Baltimore, USA

Manuel Mameli, INSERM, Paris, France

Jean-Antoine Girault, INSERM, Paris, France


Three Partial Scholarships are available for prospective participants to this Course, generously provided by the Synaptic Disease Association. Applicants should address their request to the Association officials and send it to:
This e-mail address is being protected from spambots. You need JavaScript enabled to view it
before April 15, 2014, including their CV and a letter of motivation along with their prospective travel costs.


This Course will be focused on understanding how drug-evoked synaptic plasticity in several brain areas reshapes circuit function and drives drug-adaptive behavior. Recently much progress in this domain has been possible due to important methodological advancements. Among these, the use of optogenetic manipulation that allows the control of neural activity in awake, behaving animals and in vivo normalization of synaptic transmission in animals with prior exposure to drugs that can erase drug-adaptive behavior have proven valuable tools. Additionally, conditional and inducible knockout mice have been instrumental to identify key molecules involved and improved understanding of the anatomy has allowed to delineate with unprecedented precision the neural circuits involved following exposure to drugs.

Addiction is a disease that manifests with compulsive drug-seeking and relapse even after prolonged withdrawal and it represents an especially useful platform to investigate the causal relationship between neural and behavioral adaptations. Although addictive drugs have in common that they converge to increase mesolimbic dopamine levels, after the drugs have been cleared from the organism a myriad of neuroadaptive traces can be observed, from altered gene regulation (eg. NF-kappaB or CREB) to cellular changes (e.g. potentiated excitatory synaptic transmission or altered spine density). It is well known that even weeks after withdrawal, one single cue may be sufficient to trigger strong drug-seeking behavior: cutting-edge research aimed at the identification of the causal relationship between the biochemical changes and the behavior observed will be a major focus of the Course program. Discussion will also be devoted to sophisticated animal models mimicking the stochastic nature of drug addiction that have helped model individual vulnerability.

The Course will provide a comprehensive review of the current research in the field and the distinguished Faculty will provide different and complementary approaches and will address key issues of frontier research. The lectures will be interactive, balancing established facts with current open questions with emphasis on the investigation methods. These will integrate with programmed discussion sessions as well as opportunities for informal gatherings designed to foster interdisciplinary collaboration as well as the discussion of new ideas between participants and Faculty that will lead to stimulating collaborations.