Primary Utricle Structure of Six Halimeda Species and Potential Relevance for Ocean Acidification Tolerance

Variations in utricle morphology may be responsible for different tolerances to ocean acidification (OA) within the macroalgal genus Halimeda, an important sediment producer on reefs. However, differences in species’ utricle morphology and their relationship to calcification and crystal formation have not been well articulated. In the present study, we characterized the utricle morphologies of six Halimeda species. Primary utricle ultrastructure was quantitatively and qualitatively compared to tissue inorganic content and crystal microstructure. Morphologies differed across species and several morphometric relationships were revealed. Primary utricle size (r2=0.70) and diffusion pathway length (r2=0.87) had inverse relationships with inorganic content based on regression analyses, and corresponded to crystal microstructure form. Species with large utricles and long diffusion pathways contained more narrow (~0.15 μm) aragonite needles and minimal micro-anhedral crystal formations. In contrast, species with small utricles and short diffusion pathways elucidated aggregates of micro-anhedral crystals and wider aragonite needles (~0.30 μm). Species’ utricle characteristics generally corresponded to specific evolutionary lineages. Thus, characteristics of Halimeda utricle morphology may control long-term adaptive responses to OA, an idea articulated in the broader literature

Retrograde Synaptic Signaling Mediated by K+ Efflux through Postsynaptic NMDA Receptors

SummarySynaptic NMDA receptors (NMDARs) carry inward Ca2+ current responsible for postsynaptic signaling and plasticity in dendritic spines. Whether the concurrent K+ efflux through the same receptors into the synaptic cleft has a physiological role is not known. Here, we report that NMDAR-dependent K+ efflux can provide a retrograde signal in the synapse. In hippocampal CA3-CA1 synapses, the bulk of astrocytic K+ current triggered by synaptic activity reflected K+ efflux through local postsynaptic NMDARs. The local extracellular K+ rise produced by activation of postsynaptic NMDARs boosted action potential-evoked presynaptic Ca2+ transients and neurotransmitter release from Schaffer collaterals. Our findings indicate that postsynaptic NMDAR-mediated K+ efflux contributes to use-dependent synaptic facilitation, thus revealing a fundamental form of retrograde synaptic signaling

歯周組織由来細胞の液性因子による間葉系幹細胞の骨分化制御

内容の要旨 , 審査の要旨広島大学(Hiroshima University)博士(歯学)Philosophy in Dental Sciencedoctora