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Kuroki, S.

Publications and source records attributed to Kuroki, S..

2 recordsLinked to original sources

Common features in plastic changes rather than constructed structures in recurrent neural network prefrontal cortex models

We have flexible control over our cognition depending on the context or surrounding environments. The prefrontal cortex (PFC) controls this cognitive flexibility; however, the detailed underlying mechanisms remain unclear. Recent developments in machine learning techniques have allowed simple recurrent neural network PFC models to perform human- or animal-like behavioral tasks. These systems allow us to acquire parameters, which we could not in biological experiments, for performing the tasks. We compared four models, in which a flexible cognition task, called context-dependent integration task, was performed; subsequently, we searched for common features. In all the models, we observed that high plastic synapses were concentrated in the small neuronal population and the more concentrated neuronal units contributed further to the performance. However, there were no common properties in the constructed structures. These results suggest that plastic changes can be more general and important to accomplish cognitive tasks than features of the constructed structures.

neuroscience

Caspase-8, RIPK1, and RIPK3 Coordinately Regulate Retinoic Acid-Induced Cell Differentiation and Necroptosis

Caspase-8, which is essential for death receptor-mediated apoptosis, inhibits necroptosis by suppressing the function of RIPK1 and RIPK3 to activate MLKL. We show that knockdown of caspase-8 expression in embryoid bodies derived from ES cells markedly enhances retinoic acid (RA)-induced cell differentiation and necroptosis, both of which are dependent on Ripkl and Ripk3. RA treatment obviously enhanced the expression of RA-specific genes having a retinoic acid response element (RARE) to induce cell differentiation, and induced marked expression of RIPK1, RIPK3 and MLKL to stimulate necroptosis. Caspase-8 knockdown induced RA receptor (RAR) to form a complex with RIPK1 and RIPK3 in the nucleus, and RAR interacting with RIPK1 and RIPK3 showed much stronger binding activity to RARE than RAR without RIPK1 or RIPK3. In Caspase-8-deficient mouse embryos, expression of RA-specific genes was obviously enhanced. Thus, caspase-8, RIPK1, and RIPK3 regulate RA-induced cell differentiation and necroptosis both in vitro and in vivo.

cell biology