Wim Crusio

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Wim E. Crusio
File:WimCrusio.jpg
Wim Crusio, August 2006
Born (1954-12-20) 20 December 1954 (age 69)
Bergen op Zoom, The Netherlands
Residence Pompignac, France
Citizenship Dutch
Fields behavioral and neural genetics, behavioral neuroscience
Institutions Radboud University Nijmegen, University of Heidelberg, French National Centre for Scientific Research (CNRS; Paris, Orleans, and Talence (Bordeaux)), University of Massachusetts Medical School
Alma mater Radboud University Nijmegen
Doctoral advisor Hans van Abeelen
Other academic advisors Bram van Overbeeke,
Hendrik de Wit,
Victor Westhoff
Doctoral students Laure Jamot,
Abdelkader Lagmouch,
Yann Mineur,
Maude Bernardet
Other notable students Frans Sluyter
Known for Behavioral neurogenetics of the hippocampus, mouse models of neuropsychiatric disorders
Notable awards IBANGS Distinguished Service Award
Author abbrev. (botany) Crusio

Wim E. Crusio is a Dutch behavioral neurogeneticist and a directeur de recherche (research director) with the French National Centre for Scientific Research in Talence, France.

Education and career

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 Ph.D. in 1979 and 1984, respectively.[1] For his master's degree, he performed research in behavior genetics,[2] plant taxonomy,[3] and vegetation science.[4] His Anubias revision continues to generate interest.[5] His work in plant taxonomy continued for several more years, with publications on the genus Samolus[6][7] and the description of a new species of the Aroid genus Lagenandra, L.dewitii, in 1986.[8] 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.[9] From 1984 to 1987, Crusio worked as a postdoc at the University of Heidelberg, supported by a NATO Science Fellowship[10] and an Alexander von Humboldt Research Fellowship.[11] During 1988, Crusio spent a year in Paris, France, supported by a fellowship from the Fyssen Foundation.[12] 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.[10] 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.[10][13][14] He is currently adjunct director of the Institut de Neurosciences Cognitives et Intégratives d'Aquitaine.[15]

Research

Exploratory behavior

When confronted with a novel environment, animals from non-sessile non-predatory animal species will often engage in exploratory behavior. Together with his mentor Hans van Abeelen, Crusio hypothesized that, on one hand, this would be advantageous (as it would enable animals to find resources, such as water, food, etc.), but, on the other hand, disadvantageous (because moving around in unfamiliar territory will render an animal vulnerable to predation).[16] Such stabilizing selection would be expected to lead to a genetic architecture characterized by ambidirectional dominance.[17] This was indeed found both for mice[16][18][19] and for Paradise fish.[20]

Hippocampal mossy fibers

During his postdoc, Crusio became interested in the inheritance of neuroanatomical variations in the mouse hippocampus, showing that about 50% of the variation found between different inbred mouse strains in the sizes of their intra- and infrapyramidal mossy fiber (IIPMF) projections could be attributed to heredity. It had previously been shown by Herbert Schwegler and Hans-Peter Lipp that these variations are correlated with the capacity of mice to master a two-way active avoidance task, animals with smaller projections learning much faster than animals with larger IIPMF.[21][22] Together with Schwegler and Lipp, Crusio showed that an inverse correlation, that is, animals with larger IIPMF learning better, could be found for spatial learning in a radial arm maze task.[23][24][25] This correlation was amenable to experimental manipulation by inducing early postnatal hyperthyroidy by injecting pups with thyroxine, which results in an enlargement of the IIPMF projection.[26] As expected, when mice from a strain with scant IIPMF projections were rendered hyperthyroid, they showed enlarged IIPMF and improved learning ability on the radial maze.[27][28] Taken together, Crusio and collaborators think that it is highly likely that this correlation is causal,[29] although this is not universally accepted.[30]

Mouse model of depression

When mice are exposed to unpredictable chronic mild stress (UCMS), they start exhibiting symptoms reminiscent of major depressive disorder in humans.[31] As it had been suggested that deficits in hippocampal neurogenesis might underlie depression,[32] 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,[33] anxiety,[34][35] depressive-like behaviors,[34] and learning,[36] with a concomitant drop in neurogenesis.[36] 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.[36]

Mouse model of autism

More recently, Crusio has been investigating the possibility that Fmr1 knockout mice might perhaps be used as a model for autism. This idea is based on the fact that patients suffering from the Fragile X syndrome, caused by a deficiency of the FMR1 gene often show autistic symptoms. A good mouse model for the Fragile X syndrome is available in the form of mice in which the Fmr1 gene (the mouse homologue of the human FMR1 gene) has been invalidated.[37] A review of the findings obtained with these mice in many different laboratories did indeed indicate that these animals display autistic-like symptoms,[38] especially changes in social behavior, a key symptom of autism.[39][40]

Editorial activities

Crusio is the founding editor-in-chief of Genes, Brain and Behavior.[41] The standards for the publication of mouse mutant studies that he and his co-editors developed for this journal[42] are gradually being accepted in the field.[43][44] He is an academic editor of PLoS ONE and served as associate editor of Behavioral and Brain Sciences (1991–2008) and The Scientific World Journal (2002-2011). Crusio serves or has served on the editorial boards of Behavioral and Brain Functions, Behavior Genetics (1991–1995), Behavioural Brain Research (1997–2007), BMC Neuroscience, BMC Research Notes, Frontiers in Behavioral Neuroscience, Journal of Visualized Experiments, the Mexican Journal of Scientific Research,[45] Molecular Brain, Neurogenetics (1998–2006), Physiology and Behavior, and Current Opinion in Behavioral Sciences. He edited special issues for the journals Behavior Genetics,[46] Behavioural Brain Research,[47] Physiology and Behavior (with Robert Gerlai),[48] Hippocampus (with Aryeh Routtenberg),[49] and Brain Research Bulletin (with Catherine Belzung and Robert Gerlai).[50] Together with Robert Gerlai he also edited a handbook on molecular genetic techniques for behavioral neuroscience.[51][52][53] Currently, he is editing the Cambridge Handbooks in Behavioral Genetics, a series of handbooks published by Cambridge University Press,[54] of which the first volume, Behavioral Genetics of the Mouse: Genetics of Behavioral Phenotypes, appeared in 2013.[55][56] Since then, two more volumes have appeared.[57]

Community service

In 1996, Crusio was one of two co-founders of the International Behavioural and Neural Genetics Society,[58] for which he served as member-at-large of the executive committee, treasurer, and president (1998–2001).[59] In 2011 he received from this society the "Distinguished Service Award",[60] which is given for exceptional contributions to the field of behavioral neurogenetics.[61] Crusio also served on the executive committees of the Behavior Genetics Association (from which he resigned in protest to Glayde Whitney's 1995 presidential address),[62][63] the European Brain and Behaviour Society,[64] and the International Behavioral Neuroscience Society,[65] and has been a President of the Dutch Behavior Genetics Contact Group.[66] He has been a member of several program committees for scientific meetings, most notably the 8th and 10th[67] World Congresses of Psychiatric Genetics and the 2008, 2009 (co-chair), 2010 (chair), and 2011 (chair) Annual Meetings of the IBNS.[68]

Significant papers

According to the Web of Science, Crusio's works have been cited over 3900 times and he has an h-index of 34.[69] Some significant papers are:

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References

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External links

  • Curriculum Vitae
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