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In the adult mouse hippocampus, NMDA receptors (NMDARs) of CA1 neurons play an important role in the synaptic plasticity. The location of NMDARs can determine their roles in the induction of long-term potentiation (LTP). However, the extrasynaptic NMDARs (ES-NMDARs) dependent LTP haven’t been reported. Here, through the use of a 5-Hz stimulation and MK-801 (an irreversible antagonist of NMDARs) in the CA1 neurons of adult mice hippocampal slices, synaptic NMDARs were selectively inhibited and NMDAR-mediated excitatory postsynaptic currents were not recovered. We found that a robust LTP was induced by 3-train 100-Hz stimulation when the synaptic NMDARs and extrasynaptic NR2B containing NMDARs were blocked, but not in the any of the following conditions: blocking of all NMDARs (synaptic and extrasynaptic), blocking of the synaptic NMDARs, and blocking of the synaptic NMDARs and extrasynaptic NR2A-containing NMDARs. The results indicate that this LTP is ES-NMDARs dependent, and NR2B-containing ES-NMDARs modulates the threshold of LTP induction.

PurposeTo analyze the biomechanics of cervical spine after one-and two-level Total Disc Replacement (TDR) and two-level Anterior Cervical Discectomy and Fusion (ACDF).MethodsSeven adult human cadaveric cervical spines were biomechanically evaluated under eccentric displacement control in six mechanical modes, including flexion (Flex), extension (Ext), left bending (LB), right rending (RB), left rotation (LR) and right rotation (RR).ResultsIn fusion-treated specimens, range of motion (ROM) at instrumented level decreased as much as 81.78%, and other levels also demonstrated big difference in ROM. In arthroplasty-treated specimens, ROM showed little difference from that of the intact state. Large motion variation happened in LB, RB and Ext after both fusion and nonfusion surgical treatments.ConclusionsTDR had a more reasonable motion sharing than ACDF, especially in Flex, Ext, LR and RR. No evident influence of motion change was observed after adding an extra level of TDR.

The potential to exhibit synaptic plasticity itself is modulated by previous synaptic activity, which has been termed as metaplasticity. In this paper, we demonstrated that the activation of N-methyl- d -aspartate (NMDA) receptor 2B (NR2B) subunit in NNDA receptors was required for hippocampal metaplasticity at Schaffer collateral–commissural fiber-CA1 synapses. Brief 5 Hz priming stimulation did not cause long-term synaptic plasticity; however, it could result in the inhibition of subsequently evoked long-term potentiation (LTP). Meanwhile, the application of selective antagonists for NR2B subunit of NMDA receptors after delivering priming stimulation could block the metaplasticity. In contrast, LTP induction was not affected by NR2B antagonists in slices without pre-treatment of priming stimulation. These results indicated that the activation of NR2B-containing NMDA receptors was required for metaplasticity.