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Murayama, E.

Publications and source records attributed to Murayama, E..

5 recordsLinked to original sources

Sleep neural code perpetuates the evolving negativity bias under stress

Negativity bias is the distorted cognitive processing of how self-experiences are negatively perceived through rumination and overgeneralization. Despite proposed theories of higher-order emotional representation and the involvement of default mode networks, the biological mechanisms underlying how negative emotional bias is persistently generated remain unknown. Here, we show that under negative emotional state, sleep orchestrates neural dynamics to shape persistent negativity bias. A negative emotional state, induced by repeated social defeat stress (SoD), generates negativity bias in both memory-recall and novel experiences such as fear conditioning. Longitudinal Ca2+ imaging of the hippocampus across days revealed that in emotional states, negative schema-like representations that encode the semantic aspect of negativity across experiences are generated. These negative schema-like representations are continuously processed along with dynamic co-reactivations of distinct emotional experiences during sleep. Closed-loop optogenetic silencing of stress experience-tagged cellular ensembles during sleep, but not during awake, prevents negativity bias in future memory-recall and novel experiences. Finally, sleep-active, but not sleep-nonactive, SoD cells predict and decode emotional behaviours during learned and novel situations. Together, these results reveal the biological emergence of semantic-like representations of emotional experiences and sleep causally coordinate neuronal dynamics to persistently shape negativity in future conscious states. These findings offer a new perspective on how higher-order emotional processing during sleep may determine our emotional interpretation of past and future experiences.

neuroscience↗

Alcam-a and Pdgfr-α are essential for the development of sclerotome derived stromal cells that support hematopoiesis in vivo.

Mesenchymal stromal cells are essential components of hematopoietic stem and progenitor cell (HSPC) niches, regulating HSPC proliferation and fate decisions. Their developmental origins are largely unknown. In zebrafish, we previously found that the stromal cells of the caudal hematopoietic tissue (CHT), a niche functionally homologous to the fetal liver in mammals, arise from the ventral part of caudal somites. We have now discovered that this ventral domain is actually the sclerotome, and that two typical markers of mammalian mesenchymal stem/stromal cells, Alcam and Pdgfr-, are distinctively expressed there and instrumental for the emergence and migration of stromal cell progenitors, which in turn conditions the proper assembly of the vascular component of the CHT niche. Furthermore, we find that the trunk somites are similarly dependent on Alcam and Pdgfr- to produce mesenchymal stromal cells that foster the initial emergence of HSPCs from the dorsal aorta. Thus the sclerotome contributes essential stromal cells for each of the key steps of developmental hematopoiesis, and likely is the embryological origin of most if not all mesenchymal stem/stromal cells found in non-cephalic tissues.

developmental biology↗

The hippocampus as a sorter and reverberatory integrator of sensory inputs

In entorhinal-hippocampal networks, the trisynaptic pathway, including the CA3 recurrent circuit, processes episodes of context and space1-3. Recurrent connectivity can generate reverberatory activity4-6, an intrinsic activity pattern of neurons that occurs after sensory inputs have ceased. However, the role of reverberatory activity in memory encoding remains incompletely understood. Here we demonstrate that in mice, synchrony between conditioned stimulus (CS) and unconditioned stimulus (US)-responsible cells occurs during the reverberatory phase, lasting for approximately 15 s, but not during CS and US inputs, in the CA1 and the reverberation is crucial for the linking of CS and US in the encoding of delay-type cued-fear memory. Retrieval-responsive cells developed primarily during the reverberatory phase. Mutant mice lacking N-methyl-D-aspartate receptors (NRs) in CA3 showed a cued-fear memory impairment and a decrease in synchronized reverberatory activities between CS- and US-responsive CA1 cells. Optogenetic CA3 silencing at the reverberatory phase during learning impaired cued-fear memory. Our findings suggest that reverberation recruits future retrieval-responsive cells via synchrony between CS- and US-responsive cells. The hippocampus uses reverberatory activity to link CS and US inputs, and avoid crosstalk during sensory inputs.

neuroscience↗

A dual involvement of Protocadherin-18a in stromal cell development guides the formation of a functional hematopoietic niche.

Hematopoietic stem and progenitor cells (HSPCs) emerge from the aorta and migrate to the caudal hematopoietic tissue (CHT) of zebrafish larvae, the hematopoietic equivalent of the mammalian fetal liver, for their proliferation and differentiation. We previously reported that somite-derived stromal cells were a key component of the CHT niche. Here we found that the cell adhesion protein protocadherin-18a (Pcdh18a) is expressed in the stromal cell progenitors (SCPs) emigrating from somites toward the future CHT. Deletion of most of the intracellular domain of Pcdh18a caused a decrease in the number of SCPs, the directionality of their migration, and the cell-contact mediated repulsion that normally occurs between migrating SCPs. These defects were followed by abnormal morphogenesis of the venous plexus that forms the CHT framework, and the inability of the resulting CHT to function as a niche for HSPCs. Finally, we found that the extracellular domain of Pcdh18a mediates trans heterophilic adhesion of stromal cells to endothelial cells in vivo and thereby the reticular vs. perivascular fate of SCPs. Our study demonstrates that Pcdh18a expression in SCPs is essential for the proper development of the hematopoietic niche.

developmental biology↗

Cortical cell ensemble control of past experience-dependent memory updating

When processing current sensory inputs, animals refer to related past experiences. Current information is then incorporated into the related neural network to update previously stored memories. However, the neuronal mechanism underlying the impact of memories of prior experiences on current learning is not well understood. Here, we found that a cellular ensemble in the posterior parietal cortex (PPC) that is activated during past experience mediates an interaction between past and current information to update memory through a PPC-anterior cingulate cortex circuit in mice. Moreover, optogenetic silencing of the PPC ensemble immediately after retrieval dissociated the interaction without affecting individual memories stored in the hippocampus and amygdala. Thus, a specific subpopulation of PPC cells represents past information and instructs downstream brain regions to update previous memories.

neuroscience↗