The phenomenon of cerebellar long-term depression (LTD), a decrease of synaptic strength between the parallel fibers (PFs) and Purkinje cells after conjunctive activation of PFs and the climbing fibers (CFs), is implicated as a cellular mechanism for motor learning. We have characterized a field-potential recording technique in cerebellar slice and have used the technique to examine the temporal conditions for cerebellar LTD induction in an attempt to examine the relevance of LTD to associative conditioning, lntersttmulus intervals (ISis) between onsets of PF and CF activation and the number of paired stimuli (pairings) were examined. LTD has distinct temporal specificity that seems to be constrained by inhibitory interneurons and can be masked by excessive stimulation. When 100 paired stimuli were given to PFs and CFs, LTD was induced with an ISI of 250 msec (PF activation preceding CF activation). In contrast, a smaller forward (125 msec), simultaneous (0 msec), or backward (-250 msec) ISis were not effective for inducing LTD. However, the blockade of GABA A receptor-mediated inhibition made it possible to induce LTD
Actinobacillus actinomycetemcomitans is associated with localized aggressive periodontitis, a disease characterized by rapid loss of the alveolar bone surrounding the teeth. Receptor activator of NF-B Ligand (RANKL) and osteoprotegerin (OPG) are two molecules that regulate osteoclast formation and bone resorption. RANKL induces osteoclast differentiation and activation, whereas OPG blocks this process by acting as a decoy receptor for RANKL. The purpose of this study was to investigate the effect of A. actinomycetemcomitans on the expression of RANKL and OPG in human gingival fibroblasts and periodontal ligament cells. RANKL mRNA expression was induced in both cell types challenged by A. actinomycetemcomitans extract, whereas OPG mRNA expression remained unaffected. Cell surface RANKL protein was also induced by A. actinomycetemcomitans, whereas there was no change in OPG protein secretion. A cytolethal distending toxin (Cdt) gene-knockout strain of A. actinomycetemcomitans did not induce RANKL expression, in contrast to its wild-type strain. Purified Cdt from Haemophilus ducreyi alone, or in combination with extract from the A. actinomycetemcomitans cdt mutant strain, induced RANKL expression. Pretreatment of A. actinomycetemcomitans wild-type extract with Cdt antiserum abolished RANKL expression. In conclusion, A. actinomycetemcomitans induces RANKL expression in periodontal connective tissue cells. Cdt is crucial for this induction and may therefore be involved in the pathological bone resorption during the process of localized aggressive periodontitis.
This study examined the effect of oral food consumption on the prevalence and levels of subgingival bacteria and yeasts in 20 gastrostomy tube‐fed children and 24 healthy controls. Microbial identification was carried out using anaerobic culture and 16S rRNA‐based PCR identification methods. Streptococcal and Actinomyces species were recovered from 100% and 76% of all subjects and averaged 66% and 11% of total cultivable organisms, respectively. In decreasing order of prevalence, Fusobacterium, enteric rods, Prevotella intermedia/Prevotella nigrescens, Capnocytophaga, Propionibacterium, yeasts, Actinobacillus actinomycetemcomitans, coagulase‐negative Staphylococcus, Campylobacter rectus, Bacteroides forsythus, and Porphyromonas gingivalis were detected in 48% to 2% of the study subjects. The cultivable levels of these species varied widely among subjects. PCR detection showed C. rectus and Eikenella corrodens both to occur in 93% of the study subjects and to be the most prevalent putative periodontal pathogens examined. In decreasing order of prevalence, PCR identified Treponema denticola, A. actinomycetemcomitans, P. nigrescens, P. intermedia, B. forsythus, and P. gingivalis in 38% to 21% of the subjects studied. Tube‐fed children and healthy controls exhibited similar subgingival microbial compositions. It appears from this study that oral food consumption is not a major determinant for the establishment of subgingival microbiota in children. J Periodontol 1997;68:1163–1168.
27The nervous system confronts challenges during development and experience that can 28 destabilize information processing. To adapt to these perturbations, synapses homeostatically 29 adjust synaptic strength, a process referred to as homeostatic synaptic plasticity. At the 30 Drosophila neuromuscular junction, inhibition of postsynaptic glutamate receptors activates 31 retrograde signaling that precisely increases presynaptic neurotransmitter release to restore 32 baseline synaptic strength. However, the nature of the underlying postsynaptic induction 33 process remains enigmatic. Here, we designed a forward genetic screen to identify factors 34 necessary in the postsynaptic compartment to generate retrograde homeostatic signaling. This 35 approach identified insomniac (inc), a gene that encodes a putative adaptor for the Cullin-3 36 ubiquitin ligase complex and is essential for normal sleep regulation. Intriguingly, we find that 37Inc rapidly traffics to postsynaptic densities and is required for increased ubiquitination following 38 acute receptor inhibition. Our study suggests that Inc-dependent ubiquitination, 39 compartmentalized at postsynaptic densities, gates retrograde signaling and provides an 40 intriguing molecular link between the control of sleep behavior and homeostatic plasticity at 41 synapses. 42 43 homeostatically enhance neurotransmitter release during PHP (Kiragasi et al., 2017; Li et al., 70 2018c;Weyhersmuller et al., 2011). Furthermore, candidate molecules 71 involved in retrograde signaling have been proposed (Orr et al., 2017;Wang et al., 2014). 72However, despite these significant insights, forward genetic screens have failed to shed light on 73 the postsynaptic mechanisms that induce retrograde signaling, a process that remains 74 enigmatic Goel et al., 2017;Hauswirth et al., 2018). 75 Little is known about the signal transduction system in the postsynaptic compartment 76 that initiates retrograde homeostatic communication. It is clear that pharmacological blockade or 77 genetic loss of GluRIIA-containing receptors initiates retrograde PHP signaling. Perturbation of 78 these receptors lead to reduced levels of active (phosphorylated) Ca 2+ /calmodulin-dependent 79 protein kinase II (CaMKII) (Goel et al., 2017; Haghighi et al., 2003; Li et al., 2018c; Newman et 80 al., 2017). However, inhibition of postsynaptic CaMKII activity alone is not sufficient to induce 81 PHP expression (Haghighi et al., 2003), suggesting that additional signaling in the postsynaptic 82 compartment is required to generate retrograde communication. Furthermore, rapid PHP 83 signaling induced by pharmacological receptor blockade does not require new protein synthesis 84 (Frank et al., 2006; Goel et al., 2017). Finally, CaMKII signaling is compartmentalized at 85 postsynaptic densities, where PHP can be expressed with specificity at synapses with 86 diminished receptor function (Li et al., 2018b; Newman et al., 2017), suggesting that retrograde 87 communication happens locally between individual pre-and post-s...
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