In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

[EX Q]: Context: Sigma-1 receptors are involved in the pathophysiological process of several neuropsychiatric diseases such as epilepsy, depression. Allosteric modulation represents an important mechanism for receptor functional regulation. In this study, we examined antidepressant activity of the latest identified novel and selective allosteric modulator of sigma-1 receptor 3-methyl-phenyl-2, 3, 4, 5-tetrahydro-1H-benzo[d]azepin-7-ol (SOMCL-668).', 'A single administration of SOMCL-668 decreased the immobility time in the forced swimming test (FST) and tailing suspended test in mice, which were abolished by pretreatment of sigma-1 receptor antagonist BD1047. In the chronic unpredicted mild stress (CUMS) model, chronic application of SOMCL-668 rapidly ameliorated anhedonia-like behavior (within a week), accompanying with the enhanced expression of brain-derived neurotrophic factor (BDNF) and phosphorylation of glycogen synthase kinase 3β (GSK3β) (Ser-9) in the hippocampus. SOMCL-668 also rapidly promoted the phosphorylation of GSK3β (Ser-9) in an allosteric manner in vitro. In the cultured primary neurons, SOMCL-668 enhanced the sigma-1 receptor agonist-induced neurite outgrowth and the secretion of BDNF.\Question: Does allosteric Modulation of Sigma-1 Receptors elicit Rapid Antidepressant Activity?
[EX A]: SOMCL-668, a novel allosteric modulator of sigma-1 receptors, elicits a potent and rapid acting antidepressant effect. The present data provide the first evidence that allosteric modulation of sigma-1 receptors may represent a new approach for antidepressant drug discovery.

[EX Q]: Context: Remote renal ischemia-reperfusion injury (IRI) following infra-renal aortic occlusion leads to acute kidney injury and systemic inflammation. Hydrogen sulfide is a mediator of IRI and can ameliorate tissue injury in many organ systems. Its role in vascular surgery has yet to be established. We assessed the role of hydrogen sulfide in a rodent model of aortic occlusion.', 'Wistar rats were divided into sham, control, and treatment groups (n = 6). Inflammation was assessed using a nonrecovery protocol. The infra-renal aorta was cross-clamped for 60 min and animals were reperfused for 120 min. Ten minutes before clamp release, treatment animals received hydrogen sulfide (10, 30, or 50 μg/kg) and control animals received 0.9% saline injected into the retroperitoneum. Renal injury and histology were assessed by a recovery protocol. The procedure was identical to the nonrecovery arm but with a single dose of hydrogen sulfide (30 μg/kg) and animals were recovered for 7 days.', 'There was no difference in animal weight between the groups (P = 0.337). In the nonrecovery arm, there was a reduction in serum levels of tumor necrosis factor alpha in sulfide-treated animals compared with controls (909 ± 98 vs. 607 ± 159 pg/mL; P = 0.0038). There was also a reduction in myeloperoxidase-positive cells in renal tissue in the sulfide-treated animals compared with controls (8 ± 4 vs. 17 ± 9; P = 0.03). There was no difference in histological injury score or endothelin-1 levels. In the recovery arm, there was no difference in renal function, Kidney Injury Molecule-1 levels, or histological injury scores.\Question: Does hydrogen sulfide reduce inflammation following abdominal aortic occlusion in rats?
[EX A]: Hydrogen sulfide has systemic and renal anti-inflammatory effects in remote IRI following aortic occlusion in rats.

[EX Q]: Context: Water channel aquaporin (AQP)-4 is expressed in Muller cells in retina, which are similar to astroglial cells in the central nervous system, where AQP4 deletion protects against cytotoxic brain edema after cerebral ischemia. A transient ischemia-reperfusion model was used to determine whether AQP4 deletion in mice protects the retina.', 'Retinal function and morphology were assessed in wild-type versus AQP4-deficient mice after ischemic damage produced by a 45- to 60-minute elevation of intraocular pressure to 120 mm Hg. Retinal function was assessed by electroretinography, and retinal structure by light microscopy. Extracellular space (ECS) size in fluorescently stained retinal slices was assessed by fluorescence recovery after photobleaching.', 'Retinal function and cell survival were significantly improved in AQP4-deficient mice in both inbred (C57/bl6) and outbred (CD1) genetic backgrounds. By electroretinography, b-wave amplitude was reduced by 75% to 83% at 1 to 4 days after ischemia in wild-type mice versus 48% to 51% in AQP4-null CD1 mice. Reductions were 53% to 72% versus <34% in C57/bl6 mice. Retinal structure and cell count were preserved in AQP4-null mice, particularly in the inner nuclear and plexiform layers of the retina, where Müller cells are concentrated. At 4 days after ischemia, inner retinal thickness was thinned by 43% in wild-type mice versus 11% in AQP4-null mice. Several mechanisms for retinal protection were investigated, including ECS expansion, reduced early swelling, and altered Kir4.1 K(+) channel expression.\Question: Does aquaporin-4 gene disruption in mice protect against impaired retinal function and cell death after ischemia?
[EX A]:
AQP4 deletion in mice is neuroprotective in a transient ischemia model of retinal injury, suggesting the possible use of AQP4 inhibitors in retinal vascular occlusive and ischemic diseases.