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Activation of transient receptor potential vanilloid 4 (TRPV4) induces neuronal injury. TRPV4 activation enhances inflammatory response and promotes the proinflammatory cytokine release in various types of tissue and cells. Hyperneuroinflammation contributes to neuronal damage in epilepsy. Herein, we examined the contribution of neuroinflammation to TRPV4-induced neurotoxicity and its involvement in the inflammation and neuronal damage in pilocarpine model of temporal lobe epilepsy in mice. Icv. injection of TRPV4 agonist GSK1016790A (GSK1016790A-injected mice) increased ionized calcium binding adapter molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) protein levels and Iba-1-positive (Iba-1+) and GFAP-positive (GFAP+) cells in hippocampi, which indicated TRPV4-induced microglial cell and astrocyte activation. The protein levels of nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3) inflammasome components NLRP3, apoptosis-related spotted protein (ASC) and cysteinyl aspartate-specific protease-1 (caspase-1) were increased in GSK1016790A-injected mice, which indicated NLRP3 inflammasome activation. GSK1016790A also increased proinflammatory cytokine IL-1β, TNF-α and IL-6 protein levels, which were blocked by caspase-1 inhibitor Ac-YVAD-cmk. GSK1016790A-induced neuronal death was attenuated by Ac-YVAD-cmk. Icv. injection of TRPV4-specific antagonist HC-067047 markedly increased the number of surviving cells 3 d post status epilepticus in pilocarpine model of temporal lobe epilepsy in mice (pilocarpine-induced status epilepticus, PISE). HC-067047 also markedly blocked the increase in Iba-1 and GFAP protein levels, as well as Iba-1+ and GFAP+ cells 3 d post-PISE. Finally, the increased protein levels of NLRP3, ASC and caspase-1 as well as IL-1β, TNF-α and IL-6 were markedly blocked by HC-067047. We conclude that TRPV4-induced neuronal death is mediated at least partially by enhancing the neuroinflammatory response, and this action is involved in neuronal injury following status epilepticus.

Activation of transient receptor potential vanilloid 4 (TRPV4) induces neuronal injury. TRPV4 activation enhances inflammatory response and promotes the proinflammatory cytokine release in various types of tissue and cells. Hyperneuroinflammation contributes to neuronal damage in epilepsy. Herein, we examined the contribution of neuroinflammation to TRPV4-induced neurotoxicity and its involvement in the inflammation and neuronal damage in pilocarpine model of temporal lobe epilepsy in mice. Icv. injection of TRPV4 agonist GSK1016790A (GSK1016790A-injected mice) increased ionized calcium binding adapter molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) protein levels and Iba-1-positive (Iba-1

Epilepsy is characterized by spontaneous seizures. Changes in the expression of the connexins (Cxs) have been reported to be involved in epileptogenesis. It has previously been shown that the transient receptor potential vanilloid 4 (TRPV4) plays an important role in the modulation of neuronal excitability, and that application of a TRPV4 antagonist blocks hyperthermia-induced seizures. Accordingly, in the present study, we sought to explore whether TRPV4 is involved in the regulation of Cx expression following pilocarpine-induced status epilepticus (PISE) in mice. We observed that TRPV4 protein levels in hippocampi increased 3 h to 30 d following PISE, peaking 1–3 d after induction, and that pre-application of the TRPV4 antagonist HC-067047 increased the latency to develop SE induced by pilocarpine and reduced the success rate of PISE preparation. We demonstrated that Cx43 protein levels followed a time profile similar to that of TRPV4, and further showed that the increase in Cx43 protein levels on 3 d post-PISE was markedly attenuated by HC-067047. In contrast, the corresponding increase in Cx32 protein levels lagged substantially behind, and these levels were unaffected by HC-067047. Similarly, the TRPV4 agonist GSK1016790A increased the mRNA and protein levels of Cx43, but not those of Cx32. We thus conclude that the upregulation of Cx43 expression by TRPV4 may be involved in the pathophysiology of epilepsy.

Background/Aims: Glycine plays an important role in regulating hippocampal inhibitory/ excitatory neurotransmission through activating glycine receptors (GlyRs) and acting as a co-agonist of N-methyl-d-aspartate-type glutamate receptors. Activation of transient receptor potential vanilloid 4 (TRPV4) is reported to inhibit hippocampal A-type γ-aminobutyric acid receptor, a ligand-gated chloride ion channel. GlyRs are also ligand-gated chloride ion channels and this paper aimed to explore whether activation of TRPV4 could modulate GlyRs. Methods: Whole-cell patch clamp recording was employed to record glycine-activated current (IGly) and Western blot was conducted to assess GlyRs subunits protein expression. Results: Application of TRPV4 agonist (GSK1016790A or 5,6-EET) increased IGly in mouse hippocampal CA1 pyramidal neurons. This action was blocked by specific antagonists of TRPV4 (RN-1734 or HC-067047) and GlyR (strychnine), indicating that activation of TRPV4 increases strychnine-sensitive GlyR function in mouse hippocampal pyramidal neurons. GSK1016790A-induced increase in IGly was significantly attenuated by protein kinase C (PKC) (BIM II or D-sphingosine) or calcium/calmodulin-dependent protein kinase II (CaMKII) (KN-62 or KN-93) antagonists but was unaffected by protein kinase A or protein tyrosine kinase antagonists. Finally, hippocampal protein levels of GlyR α1 α2, α3 and β subunits were not changed by treatment with GSK1016790A for 30 min or 1 h, but GlyR α2, α3 and β subunits protein levels increased in mice that were intracerebroventricularly (icv.) injected with GSK1016790A for 5 d. Conclusion: Activation of TRPV4 increases GlyR function and expression, and PKC and CaMKII signaling pathways are involved in TRPV4 activation-induced increase in IGly. This study indicates that GlyRs may be effective targets for TRPV4-induced modulation of hippocampal inhibitory neurotransmission.

We study the optical bistability (OB) in photonic multilayers doped by graphene sheets, stacking two Bragg reflectors with a defect layer between the reflectors. OB stems from the nonlinear effect of graphene, so the local field of defect mode (DM) could enhance the nonlinearity and reduce the thresholds of bistability. The structure achieves the tunability of bistability due to that the DM frequency and transmittance could be modulated by the chemical potential. Bistability thresholds and interval of the two stable states could be remarkably reduced by decreasing the chemical potential. A lager Bragg periodic number could increase the localizing of field, but the graphene loss may decrease the intensity of transmission light. We have concluded an appropriate periodic number to achieve OB. The study suggests that the tunable bistability of the structure could be used for all-optical switches in optical communication systems.

We investigate the nonlinear supermodes of surface plasmon polaritons in graphene multilayers with arbitrary number of graphene layers. Apart from the symmetric and anti-symmetric supermodes which exist in linear multilayer graphene waveguides, more asymmetric supermodes emerge in the nonlinear counterparts as the field symmetry is broken. The number of asymmetric supermodes relies largely on the layer number of graphene. There is a certain threshold of field intensity for the emergence of each individual asymmetric supermode. The threshold increases as the incident wavelength or chemical potential of graphene increases. The study may find applications in building all-optical mode converters and switches.

We investigate the vector plasmonic lattice solitons (PLSs) in nonlinear graphene-pair arrays (GPAs) consisting of periodically arranged double graphene sheets, which are spatially separated. There are two dispersion bands for the Bloch modes in the array due to the coupling of surface plasmon polaritons (SPPs) between the graphene pairs. The vector PLSs composed of two components originate from the nonlinear interaction of Bloch modes in different bands. Both components undergo mutual self-trapping through the balance between diffraction and self-focusing nonlinearity of graphene. Thanks to the strong confinement of SPPs, the vector PLSs can be squeezed into a lateral width of ∼λ/100. The study provides a promising approach to all-optical control on a deep-subwavelength scale.

The Chinese loess was proved a promising adsorbent for Zn(II) removal from aqueous solution with adsorption capacities at 70.2–83.2 mg g− 1 at 15–45 °C. Batch tests were conducted to evaluate the factors affecting the removal efficiency, of which the pH, temperature and initial Zn concentration all found in positive relevance to the increase of Zn(II) removal efficiency except for the slurry concentration. The uptake of Zn(II) on Chinese loess was considered as ion-exchange adsorption based on the calculated adsorption energy at − 12.8 to − 16.18 kJ mol− 1 by D–R isothermal adsorption model. The adsorption kinetics follows the pseudo-second-order kinetics and the equilibrating duration was found to be > 24 h. Thermodynamic investigation shows that the enthalpy and entropy changes during adsorption are in the range of 18.27–47.83 kJ mol− 1 and 52.7–129.6 J mol− 1 K− 1, respectively. The predicted Gibb's free energies were in the range of − 5.97–3.09 kJ mol− 1, indicating that the adsorption was in favor of higher temperature and lower initial Zn(II) concentration. The optimal Zn(II) removal efficiency could be obtained under the following conditions: low or intermediate Zn(II) concentration, long reaction time, high temperature and initial pH > 3.0.

We investigate the surface plasmonic lattice solitons (PLSs) in semi-infinite graphene sheet arrays. The surface soliton is formed as the SPPs tunneling is inhibited by the graphene nonlinearity, and meanwhile the incident power should be above a threshold value. Thanks to the strong confinement of surface plasmon polaritons (SPPs) on graphene, the effective width of surface PLSs can be squeezed into deep-subwavelength scale of ~ 0.001{\lambda}. Based on the stable propagation of surface PLSs, we find that the light propagation can be switched from the array boundary to the inner graphene sheets by reducing the incident power or increasing the chemical potential of graphene. The study may find promising application in optical switches on deep-subwavelength scale., Comment: 5 pages, 5 figures

We investigate the plasmonic lattice solitons (PLSs) in nonlinear graphene sheet arrays (GSAs) composed of spatially separated graphene sheets embedded in dielectric. Both the nonlinearities of graphene and dielectric are considered. The self-focusing PLSs at the Brillouin zone edges can be yielded by balancing the normal diffraction of surface plasmon polaritons (SPPs) via either the nonlinear effect of graphene or self-focusing dielectric. The self-defocusing PLSs corresponding to anomalous diffraction of SPPs at the Brillouin zone center could be yielded by the nonlinearity of self-defocusing dielectric alone. The width and propagation distance of the PLSs are dependent on the period of the GSAs and the chemical potential of graphene. Thanks to the strong confinement of SPPs, the PLSs in GSAs can be squeezed into an effective width as small as λ/250. The study may find applications in optical circuits and switches on deep-subwavelength scale.

We investigate the surface vector plasmonic lattice solitons (PLSs) in semi-infinite graphene-pair arrays (GPAs). The surface vector PLSs are composed of two components which are associated with different band gaps. Both components undergo mutual self-trapping at the boundary of the semi-infinite structure when the self-focusing nonlinearity of graphene and the light diffraction reach a balance. Thanks to the strong confinement of SPPs, the surface vector PLSs can be squeezed into a deep-subwavelength width of ~0.003λ. By comparing with bulk solitons, the surface PLSs are more readily to excite by external waves and more sensitive to the surrounding environment. The study may develop promising applications in all-optical switching devices and optical sensors on deep-subwavelength scale.