We have performed a comprehensive behavioral and anatomical analysis of the missing in metastasis (Mtss1/MIM) knockout (KO) mouse brain.
• MIM-Induced Membrane Bending Promotes Dendritic Spine Initiation
Saarikangas J, Kourdougli N, Senju Y,Chazal G, Segerstrale M, Minkeviciene R, Kuurne J, Mattila PK, Garrett L, Holter SM, Becker L, Racz I, Hans W, Klopstock T, Wurst W, Zimmer A, Fuchs H, Gailus-Durner V, Hrabe de Angelis M, von Ossowski L, Taira T, Lappalainen P, Rivera C and Hotulainen P (2015)
• MIM-Deficient Mice Exhibit Anatomical Changes in Dendritic Spines, Cortex Volume and Brain Ventricles, and Functional Changes in Motor Coordination and Learning
Minkeviciene R, Hlushchenko I, Virenque A, Lahti L, Khanal P, Rauramaa T, Koistinen A, Leinonen V, Noe FM and Hotulainen P (2019)
We also analyzed the expression of MIM in different brain regions at different ages. MIM is an I-BAR-containing membrane-curving protein, shown to be involved in dendritic spine initiation and dendritic branching in Purkinje cells in the cerebellum. Behavioral analysis of MIM KO mice revealed defects in both learning and reverse-learning, alterations in anxiety levels and reduced dominant behavior, and confirmed deficiency in motor coordination and pre-pulse inhibition. Anatomically, we observed enlarged brain ventricles and decreased cortical volume. Although MIM expression was relatively low in the hippocampus after early development, hippocampal pyramidal neurons exhibited reduced density of thin and stubby dendritic spines. Learning deficiencies can be connected to all detected anatomical changes. Both behavioral and anatomical findings are typical for schizophrenia mouse models.
Now we focus on early developmental changes in MIM expression and brain ventricle enlargement.