A role for mDia, a Rho-regulated actin nucleator, in tangential migration of interneuron precursors

神経細胞の配置メカニズムを解明－抑制性神経前駆細胞に特有の移動の機構が明らかに. 京都大学プレスリリース. 2012-1-16.In brain development, distinct types of migration, radial migration and tangential migration, are shown by excitatory and inhibitory neurons, respectively. Whether these two types of migration operate by similar cellular mechanisms remains unclear. We examined neuronal migration in mice deficient in mDia1 (also known as Diap1) and mDia3 (also known as Diap2), which encode the Rho-regulated actin nucleators mammalian diaphanous homolog 1 (mDia1) and mDia3. mDia deficiency impaired tangential migration of cortical and olfactory inhibitory interneurons, whereas radial migration and consequent layer formation of cortical excitatory neurons were unaffected. mDia-deficient neuroblasts exhibited reduced separation of the centrosome from the nucleus and retarded nuclear translocation. Concomitantly, anterograde F-actin movement and F-actin condensation at the rear, which occur during centrosomal and nuclear movement of wild-type cells, respectively, were impaired in mDia-deficient neuroblasts. Blockade of Rho-associated protein kinase (ROCK), which regulates myosin II, also impaired nuclear translocation. These results suggest that Rho signaling via mDia and ROCK critically regulates nuclear translocation through F-actin dynamics in tangential migration, whereas this mechanism is dispensable in radial migration

You Need Guts to Make New Neurons

PURPOSE OF THE REVIEW: In the present review, we discuss the very recent findings that the gut microbiota composition can modulate cell-based plasticity in the brain, namely, adult hippocampal neurogenesis, and thereby alter hippocampal dependent behavior. RECENT FINDINGS: Absence of gut microbiota from birth or antibiotic-induced dysbiosis in adults leads to an aberrant metabolite production and immune functions. Both scenarios compromise a proper postnatal brain development, or brain wiring in adults, including aberrant neurogenesis. This in turn leads to a hippocampal mismanagement of environmental cues and renders the animals to be more susceptible to stress and less cognitively flexible which contribute to general impairments in learning and memory functions and social behavior. SUMMARY: Mounting evidence indicates that certain behavior aberrances in germ-free and dysbiotic mice are mediated by changes in neurogenesis. The mechanisms and the relevance of this complex regulation remain to be elucidated by future research