Wim E. Crusio is a Dutch scientist working on the genetics of behavior and the nervous system. He is "directeur de recherche" (research director, a job title for a senior researcher) with the French National Centre for Scientific Research in Talence, France.
Education and career
Crusio got in 1979 a master's degree and then in 1984 a PhD from the Radboud University Nijmegen. He performed research in behavior genetics, plant taxonomy, and vegetation science for his master's degree. His revision of the genus Anubias continues to generate interest. His work in plant taxonomy continued for several more years. He wrote about the genus Samolus. In 1986 he described a new species of the Aroid genus Lagenandra, L.dewitii. Crusio studied the inheritance of the behavior of mice exploring a new environment for his PhD He also looked at the effects on this behavior of not being able to smell (anosmia). He used quantitative-genetic methods such as the diallel cross for this. Crusio worked as a postdoctoral researcher at the University of Heidelberg from 1984 to 1987. This was supported by a NATO Science Fellowship and an Alexander von Humboldt Research Fellowship. Crusio spent the year 1988 in Paris (France) supported by a fellowship from the Fyssen Foundation. He returned to Heidelberg as a senior research scientist. He was then recruited as "chargé de recherche" by the CNRS. He worked at first in an institute of the Paris Descartes University (Paris V). He was promoted to research director in 1994. In 1997 he moved to the CNRS campus in Orléans. Crusio became professor of psychiatry at the University of Massachusetts Medical School in Worcester, Massachusetts in 2000 and returned to the CNRS in 2005. He became a group leader in the "Centre de Neurosciences Intégratives et Cognitives" in Talence, a suburb of Bordeaux. He is currently adjunct director of the "Institut de Neurosciences Cognitives et Intégratives d'Aquitaine".
Research
Exploratory behavior
Animals will often explore a new environment if they have the chance. Crusio thought that this would be favorable: it would make it possible for animals to find water, food, etc. However, moving around in unfamiliar spaces is dangerous. Such stabilizing selection would leave genetic traces. Crusio did indeed find such traces for mice and for Paradise fish.
Hippocampal mossy fibers
In Heidelberg, Crusio became interested in the inheritance of variations in the neuroanatomy of the mouse hippocampus. He studied the intra- and infrapyramidal mossy fiber (IIPMF) projections in this brain area. Crusio showed that about 50% of the variation found between different inbred mouse strains in the sizes of their IIPMF were due to genetic differences. Herbert Schwegler and Hans-Peter Lipp had found that these variations are correlated with learning a two-way active avoidance task. Animals with smaller projections learned much faster than animals with larger IIPMF. Together with Schwegler and Lipp, Crusio showed that an inverse correlation could be found for spatial learning in a radial arm maze task. Animals with larger IIPMF learned better in this task. Injecting mouse pups with thyroxine results in larger IIPMF projections. When mice from a strain with small IIPMF projections zere treated in this way, they could learn better in the radial maze. Crusio and his collaborators think that this correlation is causal. Not everybody believes this.
Mouse model of depression
Mice that suffer unpredictable chronic mild stress (UCMS) show symptoms that look like depression in humans. Researchers were thinking that deficits in hippocampal neurogenesis (the birth of new nerve cells) might be the cause of depression. Crusio and collaborators did experiments to look at changes in behavior and neurogenesis in stressed mice. They showed large changes in levels of aggression, anxiety, depressive-like behaviors, and learning. At the same time, there was a large drop in neurogenesis. The results dependent very much on the strain and sex. There did not appear to be a clear-cut correlation between the different changes. They concluded that their data do not support the idea that deficits in hippocampal neurogenesis alone are the cause of depression. However, they do not disprove this hypothesis either.