Influence of relative positions of the heat carrier and lateral canal opening on gutta-percha obturation of lateral canals in a three-dimensional-printed model.

Background/purpose: Effective filling of the lateral canals is of great significance in successful root canal treatment, but it is generally being challenging. This study aimed to evaluate the influence of relative positions of the heat carrier and lateral canal opening on gutta-percha obturation of lateral canals in a three-dimensional (3D)-printed model. Materials and methods: Thermal conductivity and real-time temperature transmission of gutta-percha were investigated using laser flash and thermal infrared analyses. 3D-printed root canal models with lateral canals at 1, 3, and 5 mm from the apex were fabricated, and different relative positions of the heat carrier were tested. The obturation process was recorded on video, and the obturation depth of the lateral canals was observed using X-ray micro-computed tomography. Results: Gutta-percha showed low thermal conductivity of 1.07 W/(m·K), and heating increased the temperature of gutta-percha above 60 °C only within 1 mm beyond the heat carrier tip. For lateral canals at 1 and 3 mm from the apex, gutta-percha penetrated further with deeper penetration of the heat carrier (P < 0.05). For 5-mm lateral canals, the heat carrier was always at apical level and the gutta-percha obturation depth was more at 2 mm apically than at 3 or 4 mm (P < 0.05). Conclusion: Gutta-percha is a poor thermal conductor. The position of the heat carrier in relation to the lateral canal opening affects obturation depth. Only when the heat carrier reaches or passes the lateral canal opening can gutta-percha penetrate a lateral canal.

Acute Administration of Methyleugenol Impairs Hippocampus-Dependent Contextual Fear Memory and Increases Anxiety-like Behavior in Mice.

Methyleugenol (ME) as a natural essential oil in many plant species is widely used in human food and beverage for its fragrance and possible beneficial health effects. Previous chronic or subacute studies in rodents show that ME mainly causes liver toxicity. However, whether and how acute ME affects the central nervous system still remain elusive. Here, we found that ME administrated into the hippocampus impaired the acquisition of hippocampus-dependent contextual fear memory in mice (ME vs control: repeated-measures two-way ANOVA, F(5,70) = 2.937, p < 0.05; Fisher test, p < 0.05, respectively, 53 ± 5.2% vs 73 ± 7.6% during trial 4 and 46.8 ± 6% vs 74.5 ± 9.3% during trial 5). Meanwhile, acute ME impaired hippocampal CA1 long-term potentiation (LTP; ME vs control: independent t-test, p < 0.01, 110.6 ± 1.8% vs 133.3 ± 5.6%) while facilitated long-term depression (LTD; p < 0.01, 75.7 ± 3.4% vs 88.6 ± 1.7%) in mice brain slices and inducing a decrease in learning-dependent phosphorylation of Ser831 (ME vs control: independent t-test, p < 0.001, 0.87 ± 0.03 vs 1.23 ± 0.03) and Ser845 (p < 0.01, 0.42 ± 0.07 vs 0.97 ± 0.14) sites of excitatory glutamate AMPA receptor subunit 1 (GluA1) in the hippocampus, which may be the underlying mechanisms of impairment of hippocampus-dependent learning. In addition, intrahippocampal infusion of ME also increased anxiety-like behaviors in mice. These results suggested that acute ME impaired the hippocampus function at behavioral, cellular, and molecular levels, indicating the potential risks of ME on the central nervous system.

A Highly Energetic N-Rich Zeolite-Like Metal-Organic Framework with Excellent Air Stability and Insensitivity.

A stable N-rich aromatic ligand is employed to prepare energetic zeolite-like metal-organic frameworks. IFMC-1 shows excellent air stability, and the lowest sensitivity toward impact, friction, and electrostatic discharge and the highest predicted heat of detonation among the reported coordination polymers, and even commercial materials (such as trinitrotoluene (TNT)).

Gain in sensitivity and loss in temporal contrast of STDP by dopaminergic modulation at hippocampal synapses.

Spike-timing-dependent plasticity (STDP) is considered a physiologically relevant form of Hebbian learning. However, behavioral learning often involves action of reinforcement or reward signals such as dopamine. Here, we examined how dopamine influences the quantitative rule of STDP at glutamatergic synapses of hippocampal neurons. The presence of 20 muM dopamine during paired pre- and postsynaptic spiking activity expanded the effective time window for timing-dependent long-term potentiation (t-LTP) to at least -45 ms, and allowed normally ineffective weak stimuli with fewer spike pairs to induce significant t-LTP. Meanwhile, dopamine did not affect the degree of t-LTP induced by normal strong stimuli with spike timing (ST) of +10 ms. Such dopamine-dependent enhancement in the sensitivity of t-LTP was completely blocked by the D1-like dopamine receptor antagonist SCH23390, but not by the D2-like dopamine receptor antagonist sulpiride. Surprisingly, timing-dependent long-term depression (t-LTD) at negative ST was converted into t-LTP by dopamine treatment; this conversion was also blocked by SCH23390. In addition, t-LTP in the presence of dopamine was completely blocked by the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid, indicating that D1-like receptor-mediated modulation appears to act through the classical NMDA receptor-mediated signaling pathway that underlies STDP. These results provide a quantitative and mechanistic basis for a previously undescribed learning rule that depends on pre- and postsynaptic ST, as well as the global reward signal.

Antistress effect of TRPV1 channel on synaptic plasticity and spatial memory.

BACKGROUND: Stress is believed to exacerbate neuropsychiatric and cognitive disorders. In particular, the hippocampus, which plays critical roles in certain types of memory, including spatial memory, is exquisitely sensitive to stress. Certain types of memory are believed to depend on activity-dependent hippocampal synaptic plasticity such as long-term potentiation (LTP) and long-term depression (LTD), but stress suppresses LTP and facilitates LTD in the hippocampus and impairs spatial memory. Although the transient receptor potential vanilloid 1 (TRPV1 or VR1) is widely expressed in the hippocampus, it remains unknown whether the TRPV1 channel antagonizes the stress effects on hippocampal function. METHODS: Using the TRPV1 agonists capsaicin and resiniferatoxin and selective antagonists capsazepine and SB366791, we examined the effect of TRPV1 activation on LTP and LTD in hippocampal CA1 slices of juvenile rats. Furthermore, we examined whether the effects of acute stress on synaptic plasticity and spatial memory could be prevented by intrahippocampal or intragastric infusion of a TRPV1 agonist. RESULTS: The TRPV1 agonists capsaicin and resiniferatoxin facilitated LTP but suppressed LTD. Alterations were mediated by TRPV1 because the TRPV1 selective antagonists capsazepine and SB366791 blocked the actions of capsaicin. Acute stress suppressed LTP and enabled LTD, but the TRPV1 agonist capsaicin effectively prevented this effect. When capsaicin was intrahippocampally or intragastrically infused, the acute stress effect on impairing spatial memory retrieval was completely prevented. CONCLUSIONS: The TRPV1 channel is a potential target to facilitate LTP and suppress LTD, in turn protecting hippocampal synaptic plasticity and spatial memory retrieval from the influence of acute stress.