Group I metabotropic glutamate receptors (mGluRs) modulate postsynaptic neuronal excitability and epileptogenesis. We investigated roles of group I mGluRs on low extracellular Mg2+ concentration ([Mg2+ ]o )-induced epileptiform activity and neuronal cell death in the CA1 regions of isolated rat hippocampal slices without the entorhinal cortex using extracellular recording and propidium iodide staining. Exposure to Mg2+ -free artificial cerebrospinal fluid can induce interictal epileptiform activity in the CA1 regions of rat hippocampal slices. MPEP, a mGluR 5 antagonist, significantly inhibited the spike firing of the low [Mg2+ ]o -induced epileptiform activity, whereas LY367385, a mGluR1 antagonist, did not. DHPG, a group 1 mGluR agonist, significantly increased the spike firing of the epileptiform activity.U73122, a PLC inhibitor, inhibited the spike firing. Thapsigargin, an ER Ca2+ -ATPase antagonist, significantly inhibited the spike firing and amplitude of the epileptiform activity. Both the IP 3 receptor antagonist 2-APB and the ryanodine receptor antagonist dantrolene significantly inhibited the spike firing. The PKC inhibitors such as chelerythrine and GF109203X, significantly increased the spike firing. Flufenamic acid, a relatively specific TRPC 1, 4, 5 channel antagonist, significantly inhibited the spike firing, whereas SKF96365, a relatively non-specific TRPC channel antagonist, did not.MPEP significantly decreased low [Mg2+ ] o DMEM-induced neuronal cell death in the CA1 regions, but LY367385 did not. We suggest that mGluR 5 is involved in low [Mg2+ ]o -induced interictal epileptiform activity in the CA1 regions of rat hippocampal slices through PLC, release of Ca2+ from intracellular stores and PKC and TRPC channels, which could be involved in neuronal cell death.

Group I metabotropic glutamate receptors (mGluRs) modulate postsynaptic neuronal excitability and epileptogenesis. We investigated roles of group I mGluRs on low extracellular Mg2+ concentration ([Mg2+ ]o )-induced epileptiform activity and neuronal cell death in the CA1 regions of isolated rat hippocampal slices without the entorhinal cortex using extracellular recording and propidium iodide staining. Exposure to Mg2+ -free artificial cerebrospinal fluid can induce interictal epileptiform activity in the CA1 regions of rat hippocampal slices. MPEP, a mGluR 5 antagonist, significantly inhibited the spike firing of the low [Mg2+ ]o -induced epileptiform activity, whereas LY367385, a mGluR1 antagonist, did not. DHPG, a group 1 mGluR agonist, significantly increased the spike firing of the epileptiform activity.U73122, a PLC inhibitor, inhibited the spike firing. Thapsigargin, an ER Ca2+ -ATPase antagonist, significantly inhibited the spike firing and amplitude of the epileptiform activity. Both the IP 3 receptor antagonist 2-APB and the ryanodine receptor antagonist dantrolene significantly inhibited the spike firing. The PKC inhibitors such as chelerythrine and GF109203X, significantly increased the spike firing. Flufenamic acid, a relatively specific TRPC 1, 4, 5 channel antagonist, significantly inhibited the spike firing, whereas SKF96365, a relatively non-specific TRPC channel antagonist, did not.MPEP significantly decreased low [Mg2+ ] o DMEM-induced neuronal cell death in the CA1 regions, but LY367385 did not. We suggest that mGluR 5 is involved in low [Mg2+ ]o -induced interictal epileptiform activity in the CA1 regions of rat hippocampal slices through PLC, release of Ca2+ from intracellular stores and PKC and TRPC channels, which could be involved in neuronal cell death.

Purpose: We aimed to assess the clinical efficacy and safety of combining silodosin and solifenacin for overactive bladder (OAB) in females. Methods: A retrospective analysis of 586 females with OAB was conducted. Patients received either combination therapy (silodosin 8 mg + solifenacin 5 mg) or monotherapy (solifenacin 5 mg) for 12 weeks. Baseline and follow-up assessments included the overactive bladder symptom score (OABSS), International Prostate Symptom Score (IPSS), quality of life (QoL), maximum flow rate (Qmax), voided volume (VV), and postvoid residual urine volume (PVR). Results: Overall, 287 and 299 patients received combination therapy and monotherapy respectively. Both groups experienced significant improvements in OABSS and total IPSS after 12 weeks. The combination therapy group demonstrated a greater improvement in QoL compared to the monotherapy group (P=0.031). No significant differences were observed in Qmax or VV between the groups. However, the combination therapy group showed a significant reduction in PVR compared to the monotherapy group (P<0.001). Conclusions Combining silodosin with solifenacin significantly improved OAB symptoms and QoL in females. This combination therapy was particularly effective in reducing postvoid residual volume compared to solifenacin alone. These findings suggest that adding an alpha-blocker to antimuscarinic therapy can enhance OAB management and patient satisfaction.

Group I metabotropic glutamate receptors (mGluRs) modulate postsynaptic neuronal excitability and epileptogenesis. We investigated roles of group I mGluRs on low extracellular Mg2+ concentration ([Mg2+ ]o )-induced epileptiform activity and neuronal cell death in the CA1 regions of isolated rat hippocampal slices without the entorhinal cortex using extracellular recording and propidium iodide staining. Exposure to Mg2+ -free artificial cerebrospinal fluid can induce interictal epileptiform activity in the CA1 regions of rat hippocampal slices. MPEP, a mGluR 5 antagonist, significantly inhibited the spike firing of the low [Mg2+ ]o -induced epileptiform activity, whereas LY367385, a mGluR1 antagonist, did not. DHPG, a group 1 mGluR agonist, significantly increased the spike firing of the epileptiform activity.U73122, a PLC inhibitor, inhibited the spike firing. Thapsigargin, an ER Ca2+ -ATPase antagonist, significantly inhibited the spike firing and amplitude of the epileptiform activity. Both the IP 3 receptor antagonist 2-APB and the ryanodine receptor antagonist dantrolene significantly inhibited the spike firing. The PKC inhibitors such as chelerythrine and GF109203X, significantly increased the spike firing. Flufenamic acid, a relatively specific TRPC 1, 4, 5 channel antagonist, significantly inhibited the spike firing, whereas SKF96365, a relatively non-specific TRPC channel antagonist, did not.MPEP significantly decreased low [Mg2+ ] o DMEM-induced neuronal cell death in the CA1 regions, but LY367385 did not. We suggest that mGluR 5 is involved in low [Mg2+ ]o -induced interictal epileptiform activity in the CA1 regions of rat hippocampal slices through PLC, release of Ca2+ from intracellular stores and PKC and TRPC channels, which could be involved in neuronal cell death.

Group I metabotropic glutamate receptors (mGluRs) modulate postsynaptic neuronal excitability and epileptogenesis. We investigated roles of group I mGluRs on low extracellular Mg2+ concentration ([Mg2+ ]o )-induced epileptiform activity and neuronal cell death in the CA1 regions of isolated rat hippocampal slices without the entorhinal cortex using extracellular recording and propidium iodide staining. Exposure to Mg2+ -free artificial cerebrospinal fluid can induce interictal epileptiform activity in the CA1 regions of rat hippocampal slices. MPEP, a mGluR 5 antagonist, significantly inhibited the spike firing of the low [Mg2+ ]o -induced epileptiform activity, whereas LY367385, a mGluR1 antagonist, did not. DHPG, a group 1 mGluR agonist, significantly increased the spike firing of the epileptiform activity.U73122, a PLC inhibitor, inhibited the spike firing. Thapsigargin, an ER Ca2+ -ATPase antagonist, significantly inhibited the spike firing and amplitude of the epileptiform activity. Both the IP 3 receptor antagonist 2-APB and the ryanodine receptor antagonist dantrolene significantly inhibited the spike firing. The PKC inhibitors such as chelerythrine and GF109203X, significantly increased the spike firing. Flufenamic acid, a relatively specific TRPC 1, 4, 5 channel antagonist, significantly inhibited the spike firing, whereas SKF96365, a relatively non-specific TRPC channel antagonist, did not.MPEP significantly decreased low [Mg2+ ] o DMEM-induced neuronal cell death in the CA1 regions, but LY367385 did not. We suggest that mGluR 5 is involved in low [Mg2+ ]o -induced interictal epileptiform activity in the CA1 regions of rat hippocampal slices through PLC, release of Ca2+ from intracellular stores and PKC and TRPC channels, which could be involved in neuronal cell death.

Purpose: We aimed to assess the clinical efficacy and safety of combining silodosin and solifenacin for overactive bladder (OAB) in females. Methods: A retrospective analysis of 586 females with OAB was conducted. Patients received either combination therapy (silodosin 8 mg + solifenacin 5 mg) or monotherapy (solifenacin 5 mg) for 12 weeks. Baseline and follow-up assessments included the overactive bladder symptom score (OABSS), International Prostate Symptom Score (IPSS), quality of life (QoL), maximum flow rate (Qmax), voided volume (VV), and postvoid residual urine volume (PVR). Results: Overall, 287 and 299 patients received combination therapy and monotherapy respectively. Both groups experienced significant improvements in OABSS and total IPSS after 12 weeks. The combination therapy group demonstrated a greater improvement in QoL compared to the monotherapy group (P=0.031). No significant differences were observed in Qmax or VV between the groups. However, the combination therapy group showed a significant reduction in PVR compared to the monotherapy group (P<0.001). Conclusions Combining silodosin with solifenacin significantly improved OAB symptoms and QoL in females. This combination therapy was particularly effective in reducing postvoid residual volume compared to solifenacin alone. These findings suggest that adding an alpha-blocker to antimuscarinic therapy can enhance OAB management and patient satisfaction.

Purpose: We aimed to assess the clinical efficacy and safety of combining silodosin and solifenacin for overactive bladder (OAB) in females. Methods: A retrospective analysis of 586 females with OAB was conducted. Patients received either combination therapy (silodosin 8 mg + solifenacin 5 mg) or monotherapy (solifenacin 5 mg) for 12 weeks. Baseline and follow-up assessments included the overactive bladder symptom score (OABSS), International Prostate Symptom Score (IPSS), quality of life (QoL), maximum flow rate (Qmax), voided volume (VV), and postvoid residual urine volume (PVR). Results: Overall, 287 and 299 patients received combination therapy and monotherapy respectively. Both groups experienced significant improvements in OABSS and total IPSS after 12 weeks. The combination therapy group demonstrated a greater improvement in QoL compared to the monotherapy group (P=0.031). No significant differences were observed in Qmax or VV between the groups. However, the combination therapy group showed a significant reduction in PVR compared to the monotherapy group (P<0.001). Conclusions Combining silodosin with solifenacin significantly improved OAB symptoms and QoL in females. This combination therapy was particularly effective in reducing postvoid residual volume compared to solifenacin alone. These findings suggest that adding an alpha-blocker to antimuscarinic therapy can enhance OAB management and patient satisfaction.

Group I metabotropic glutamate receptors (mGluRs) modulate postsynaptic neuronal excitability and epileptogenesis. We investigated roles of group I mGluRs on low extracellular Mg2+ concentration ([Mg2+ ]o )-induced epileptiform activity and neuronal cell death in the CA1 regions of isolated rat hippocampal slices without the entorhinal cortex using extracellular recording and propidium iodide staining. Exposure to Mg2+ -free artificial cerebrospinal fluid can induce interictal epileptiform activity in the CA1 regions of rat hippocampal slices. MPEP, a mGluR 5 antagonist, significantly inhibited the spike firing of the low [Mg2+ ]o -induced epileptiform activity, whereas LY367385, a mGluR1 antagonist, did not. DHPG, a group 1 mGluR agonist, significantly increased the spike firing of the epileptiform activity.U73122, a PLC inhibitor, inhibited the spike firing. Thapsigargin, an ER Ca2+ -ATPase antagonist, significantly inhibited the spike firing and amplitude of the epileptiform activity. Both the IP 3 receptor antagonist 2-APB and the ryanodine receptor antagonist dantrolene significantly inhibited the spike firing. The PKC inhibitors such as chelerythrine and GF109203X, significantly increased the spike firing. Flufenamic acid, a relatively specific TRPC 1, 4, 5 channel antagonist, significantly inhibited the spike firing, whereas SKF96365, a relatively non-specific TRPC channel antagonist, did not.MPEP significantly decreased low [Mg2+ ] o DMEM-induced neuronal cell death in the CA1 regions, but LY367385 did not. We suggest that mGluR 5 is involved in low [Mg2+ ]o -induced interictal epileptiform activity in the CA1 regions of rat hippocampal slices through PLC, release of Ca2+ from intracellular stores and PKC and TRPC channels, which could be involved in neuronal cell death.

Purpose: We analyzed the choroidal thickness in the subfoveal area and area of retinal detachment (RD) in monocular primary rhegmatogenous retinal detachment (RRD) patients and compared the RD eye with the fellow eye. Methods: We retrospectively analyzed, optical coherence tomography data of both eyes at the first visit in patients who underwent surgery for monocular RRD from January 2013 to December 2016. Choroidal thickness was examined manually in the subfoveal and RD areas by two independent ophthalmologists; subjects without data from at least one of the two investigators were excluded. Results: Ninety-five subjects were included in this study. Of the 95 RD eyes, 61 (64.2%) and 44 (46.3%) eyes showed macula and fovea invasion, respectively. The subfoveal choroidal thickness was statistically significant in the RD eye compared with the fellow eye (244.7 ± 79.0 µm vs. 220.1 ± 78.9 µm; p < 0.001). Moreover, the choroidal thickness of the RD area in the RD eye was thicker compared with the non-detachment area and corresponding area in the fellow eye (273.8 ± 53.4 µm vs. 215.2 ± 44.0 µm and 233.3 ± 56.7 µm, respectively; p < 0.001). Conclusions In the primary RRD eye, the choroidal thickness in the detachment area was thicker than that of the fellow eye. Further studies are needed to investigate the mechanism of choroidal thickness change and its impact on RD.

Purpose: We analyzed the choroidal thickness in the subfoveal area and area of retinal detachment (RD) in monocular primary rhegmatogenous retinal detachment (RRD) patients and compared the RD eye with the fellow eye. Methods: We retrospectively analyzed, optical coherence tomography data of both eyes at the first visit in patients who underwent surgery for monocular RRD from January 2013 to December 2016. Choroidal thickness was examined manually in the subfoveal and RD areas by two independent ophthalmologists; subjects without data from at least one of the two investigators were excluded. Results: Ninety-five subjects were included in this study. Of the 95 RD eyes, 61 (64.2%) and 44 (46.3%) eyes showed macula and fovea invasion, respectively. The subfoveal choroidal thickness was statistically significant in the RD eye compared with the fellow eye (244.7 ± 79.0 µm vs. 220.1 ± 78.9 µm; p < 0.001). Moreover, the choroidal thickness of the RD area in the RD eye was thicker compared with the non-detachment area and corresponding area in the fellow eye (273.8 ± 53.4 µm vs. 215.2 ± 44.0 µm and 233.3 ± 56.7 µm, respectively; p < 0.001). Conclusions In the primary RRD eye, the choroidal thickness in the detachment area was thicker than that of the fellow eye. Further studies are needed to investigate the mechanism of choroidal thickness change and its impact on RD.