SURFACE TREATMENT AND EXAMINATION OF GRADE 2 AND GRADE 5 TITANIUM

Surface characteristics play an important role in the implant-bone integration that is required for the long-term reliability of dental and orthopedic implants. In this paper, we investigate the effect of acid etching on the mass reduction and roughness of grade 2 and grade 5 Ti under controlled experimental conditions. Three different etching compounds were investigated: 30% HCl, 85% H3PO4 and the compound of 30% (COOH)2 × 2H2O and 30% H2O2 in various treatment intervals under controlled temperature. Stereo microscopy, scanning electron microscopy, roughness and weight measurements were carried out on the samples. We found that neither 85% H3PO4 nor the compound of 30% (COOH)2 × 2H2O and 30% H2O2 were able to remove the machining marks from the surface of Ti discs in our experimental setting. On the other hand, etching in 30% HCl yielded even surfaces both on Ti grade 2 and 5 discs. We also found that etching at higher temperatures in 30% HCl resulted in significant mass loss

Hippocampal GABAergic Synapses Possess the Molecular Machinery for Retrograde Nitric Oxide Signaling

Nitric oxide (NO) plays an important role in synaptic plasticity as a retrograde messenger at glutamatergic synapses. Here we describe that, in hippocampal pyramidal cells, neuronal nitric oxide synthase (nNOS) is also associated with the postsynaptic active zones of GABAergic symmetrical synapses terminating on their somata, dendrites, and axon initial segments in both mice and rats. The NO receptor nitric oxide-sensitive guanylyl cyclase (NOsGC) is present in the brain in two functional subunit compositions: alpha1beta1 and alpha2beta1. The beta1 subunit is expressed in both pyramidal cells and interneurons in the hippocampus. Using immunohistochemistry and in situ hybridization methods, we describe that the alpha1 subunit is detectable only in interneurons, which are always positive for beta1 subunit as well; however, pyramidal cells are labeled only for beta1 and alpha2 subunits. With double-immunofluorescent staining, we also found that most cholecystokinin- and parvalbumin-positive and smaller proportion of the somatostatin- and nNOS-positive interneurons are alpha1 subunit positive. We also found that the alpha1 subunit is present in parvalbumin- and cholecystokinin-positive interneuron terminals that establish synapses on somata, dendrites, or axon initial segments. Our results demonstrate that NOsGC, composed of alpha1beta1 subunits, is selectively expressed in different types of interneurons and is present in their presynaptic GABAergic terminals, in which it may serve as a receptor for NO produced postsynaptically by nNOS in the very same synapse

SURFACE TREATMENT AND EXAMINATION OF GRADE 2 AND GRADE 5 TITANIUM

Surface characteristics play an important role in the implant-bone integration that is required for the long-term reliability of dental and orthopedic implants. In this paper, we investigate the effect of acid etching on the mass reduction and roughness of grade 2 and grade 5 Ti under controlled experimental conditions. Three different etching compounds were investigated: 30% HCl, 85% H3PO4 and the compound of 30% (COOH)2 × 2H2O and 30% H2O2 in various treatment intervals under controlled temperature. Stereo microscopy, scanning electron microscopy, roughness and weight measurements were carried out on the samples. We found that neither 85% H3PO4 nor the compound of 30% (COOH)2 × 2H2O and 30% H2O2 were able to remove the machining marks from the surface of Ti discs in our experimental setting. On the other hand, etching in 30% HCl yielded even surfaces both on Ti grade 2 and 5 discs. We also found that etching at higher temperatures in 30% HCl resulted in significant mass loss

The NKCC1 ion transporter modulates microglial phenotype and inflammatory response to brain injury in a cell-autonomous manner

The NKCC1 ion transporter contributes to the pathophysiology of common neurological disorders, but its function in microglia, the main inflammatory cells of the brain, has remained unclear to date. Therefore, we generated a novel transgenic mouse line in which microglial NKCC1 was deleted. We show that microglial NKCC1 shapes both baseline and reactive microglia morphology, process recruitment to the site of injury, and adaptation to changes in cellular volume in a cell-autonomous manner via regulating membrane conductance. In addition, microglial NKCC1 deficiency results in NLRP3 inflammasome priming and increased production of interleukin-1 beta (IL-1 beta), rendering microglia prone to exaggerated inflammatory responses. In line with this, central (intracortical) administration of the NKCC1 blocker, bumetanide, potentiated intracortical lipopolysaccharide (LPS)-induced cytokine levels. In contrast, systemic bumetanide application decreased inflammation in the brain. Microglial NKCC1 KO animals exposed to experimental stroke showed significantly increased brain injury, inflammation, cerebral edema, and, worse, neurological outcome. Thus, NKCC1 emerges as an important player in controlling microglial ion homeostasis and inflammatory responses through which microglia modulate brain injury. The contribution of microglia to central NKCC1 actions is likely to be relevant for common neurological disorders.Peer reviewe

Microglia modulate blood flow, neurovascular coupling, and hypoperfusion via purinergic actions

Microglia, the main immunocompetent cells of the brain, regulate neuronal function, but their contribution to cerebral blood flow (CBF) regulation has remained elusive. Here, we identify microglia as important modulators of CBF both under physiological conditions and during hypoperfusion. Microglia establish direct, dynamic purinergic contacts with cells in the neurovascular unit that shape CBF in both mice and humans. Surprisingly, the absence of microglia or blockade of microglial P2Y12 receptor (P2Y12R) substantially impairs neurovascular coupling in mice, which is reiterated by chemogenetically induced microglial dysfunction associated with impaired ATP sensitivity. Hypercapnia induces rapid microglial calcium changes, P2Y12R-mediated formation of perivascular phylopodia, and microglial adenosine production, while depletion of microglia reduces brain pH and impairs hypercapnia-induced vasodilation. Microglial actions modulate vascular cyclic GMP levels but are partially independent of nitric oxide. Finally, microglial dysfunction markedly impairs P2Y12R-mediated cerebrovascular adaptation to common carotid artery occlusion resulting in hypoperfusion. Thus, our data reveal a previously unrecognized role for microglia in CBF regulation, with broad implications for common neurological diseases

Présentation du roman de Lawrence Hill, The Book of Negroes - Aminata

GABA (gamma-aminobutyric-acid), the main inhibitory neurotransmitter in the adult brain, exerts depolarizing (excitatory) actions during development and this GABAergic depolarization cooperates with NMDARs (N-methyl-D-aspartate receptors) to drive spontaneous synchronous activity (SSA) that is fundamentally important for developing neuronal networks. Although GABAergic depolarization is known to assist in the activation of NMDARs during development, the subcellular localization of NMDARs relative to GABAergic synapses is still unknown. Here, we investigated the subcellular distribution of NMDARs in association with GABAergic synapses at the developmental stage when SSA is most prominent in mice. Using multiple immunofluorescent labeling and confocal laser-scanning microscopy in the developing mouse hippocampus, we found that NMDARs were associated with both glutamatergic and GABAergic synapses at postnatal day 6–7 and we observed a direct colocalization of GABA(A)- and NMDA-receptor labeling in GABAergic synapses. Electron microscopy of pre-embedding immunogold-immunoperoxidase reactions confirmed that GluN1, GluN2A and GluN2B NMDAR subunits were all expressed in glutamatergic and GABAergic synapses postsynaptically. Finally, quantitative post-embedding immunogold labeling revealed that the density of NMDARs was 3 times higher in glutamatergic than in GABAergic synapses. Since GABAergic synapses were larger, there was little difference in the total number of NMDA receptors in the two types of synapses. In addition, receptor density in synapses was substantially higher than extrasynaptically. These data can provide the neuroanatomical basis of a new interpretation of previous physiological data regarding the GABA(A)R-NMDAR cooperation during early development. We suggest that during SSA, synaptic GABA(A)R-mediated depolarization assists NMDAR activation right inside GABAergic synapses and this effective spatial cooperation of receptors and local change of membrane potential will reach developing glutamatergic synapses with a higher probability and efficiency even further away on the dendrites. This additional level of cooperation that operates within the depolarizing GABAergic synapse, may also allow its own modification triggered by Ca(2+)-influx through the NMDA receptors

NMDA Receptors in Hippocampal GABAergic Synapses and Their Role in Nitric Oxide Signaling

GABAergic inhibition plays a central role in the control of pyramidal cell ensemble activities, thus, any signaling mechanism that regulates inhibition is able to fine-tune network patterns. Here we provide evidence that the retrograde NO-cGMP cascade triggered by NMDA-receptor activation plays a role in the control of hippocampal GABAergic transmission in mice. GABAergic synapses express nNOS postsynaptically and NO receptors (NO-sensitive guanylyl cyclase) in the presynaptic terminals. We hypothesised that – similar to glutamatergic synapses – the Ca(2+) transients required to activate nNOS were provided by NMDA receptor activation. Indeed, administration of 5μM NMDA induced a robust nNOS-dependent cGMP production in GABAergic terminals, selectively in the CA1 and CA3c areas. Furthermore, using preembedding, postembedding and SDS-digested freeze-facture replica immunogold labeling, we provided quantitative immunocytochemical evidence that NMDAR subunits GluN1, GluN2A and GluN2B were present in most somatic GABAergic synapses postsynaptically. These data indicate that NMDARs can modulate hippocampal GABAergic inhibition via NO-cGMP signaling in an activity-dependent manner, and that this effect is sub-region specific in the mouse hippocampus

Antibodies used in the study.

<p>Antibodies used in the study.</p