Wim E. Crusio (born Wilhelmus Elisabeth Crusio on 20 December 1954) is a Dutch behavioral neurogeneticist and a directeur de recherche (research director) with the French National Centre for Scientific Research in Talence, France.
Crusio received his bachelor's degree in biology from Radboud University Nijmegen in 1975, where he went on to obtain a master's degree and then a PhD in 1979 and 1984, respectively.[1] His Anubias revision, which was originally published in 1979,[1] was translated in German[2] and continues to engender interest.[3] For his PhD thesis, Crusio studied the inheritance of the effects of anosmia on exploratory behavior of mice, and more in general the genetic architecture of exploratory behavior, using quantitative-genetic methods such as the diallel cross.[4] From 1984 to 1987, Crusio worked as a postdoc at the University of Heidelberg, supported by a NATO Science Fellowship[5] and an Alexander von Humboldt Research Fellowship.[6] During 1988, Crusio spent a year in Paris, France, supported by a fellowship from the Fyssen Foundation.[7] He then returned to Heidelberg as a senior research scientist before being recruited as chargé de recherche by the CNRS, initially working in an institute of the Université René Descartes (Paris V) and later moving to the CNRS campus in Orléans, having been promoted to directeur de recherche.[5] In 2000 he became full professor of psychiatry at the University of Massachusetts Medical School in Worcester, Massachusetts, returning to the CNRS in 2005 as a group leader in the Centre de Neurosciences Intégratives et Cognitives in Talence, a suburb of Bordeaux.[5][8][9] He is currently adjunct director of the Institut de Neurosciences Cognitives et Intégratives d'Aquitaine.[10]
Crusio and his collaborators found that neuroanatomical variations in the mouse hippocampus, in particular the sizes of their intra- and infrapyramidal mossy fibers (IIPMF) correlated with learning performance.[11] Together with Herbert Schwegler and Hans-Peter Lipp, Crusio showed that an inverse correlation, that is, animals with larger IIPMF learn better, could be found for spatial learning in a radial arm maze task.[12][13][14] Taken together, Crusio and collaborators think that it is highly likely that this correlation is causal,[15] although this is not universally accepted.[16]
When mice are exposed to unpredictable chronic mild stress (UCMS), they start exhibiting symptoms reminiscent of major depressive disorder in humans.[17] As it had been suggested that deficits in hippocampal neurogenesis might underlie depression,[18] Crusio and collaborators undertook a series of experiments investigating changes in behavior and neurogenesis in mice that had undergone UCMS. They showed dramatic changes in levels of aggression,[19] anxiety,[20][21] depressive-like behaviors,[20] and learning,[22] with a concomitant drop in neurogenesis.[22] However, the results were strain- and sex-specific and there did not appear to be a clear-cut correlation between the different changes, so that they finally concluded that although their data do not disprove the idea that deficits in hippocampal neurogenesis solely underlie the behavioral impairments observed in human psychiatric disorders such as depression, they do not provide support for this hypothesis either.[22]