Depression is a major global health burden, and current treatments are limited by delayed onset and incomplete efficacy, highlighting the need for novel, mechanism-based therapies. Chronic restraint s Show more
Depression is a major global health burden, and current treatments are limited by delayed onset and incomplete efficacy, highlighting the need for novel, mechanism-based therapies. Chronic restraint stress (CRS) induces behavioral, hormonal, and synaptic changes relevant to depression, but the role of adiponectin signaling remains unclear. Here, we examined whether the adiponectin receptor agonist AdipoRon exerts antidepressant-like effects via brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) signaling in mice subjected to 14 days of CRS. CRS produced anxiety- and depression-like behaviors, elevated plasma corticosterone, reduced circulating adiponectin, and selectively decreased hippocampal adiponectin and adiponectin receptor 2 (AdipoR2), accompanied by reduced PSD-95 and GluA1 in CA3 and the dentate gyrus (DG). AdipoRon treatment (20 mg/kg, days 8-14) prevented behavioral deficits, normalized corticosterone and adiponectin levels, and restored hippocampal AdipoR2, PSD-95, and GluA1 expression in CA3 and DG. AdipoRon also reversed CRS-induced decreases in hippocampal phosphorylated AMPK (p-AMPK), PPARα, BDNF, and phosphorylated TrkB (p-TrkB), with p-AMPK/AMPK and PPARα levels positively correlating with BDNF. Immunofluorescence confirmed BDNF recovery in CA3 and DG. Importantly, pretreatment with the TrkB antagonist ANA-12 abolished the behavioral, hormonal, and molecular effects of AdipoRon, indicating that its actions require BDNF-TrkB activation. These findings suggest that AdipoRon mitigates CRS-induced deficits via hippocampal AdipoR2-AMPK-PPARα-BDNF-TrkB signaling and highlight AdipoR2 as a promising target for depression therapy under chronic stress. Show less
This research aimed to explore the serum levels of calcium/calmodulin-dependent protein kinase II (CaMKII) in hyperventilation syndrome (HVS) patients and its correlation with psychological disorders. Show more
This research aimed to explore the serum levels of calcium/calmodulin-dependent protein kinase II (CaMKII) in hyperventilation syndrome (HVS) patients and its correlation with psychological disorders. This prospective observational study enrolled 168 HVS patients who came to our hospital from February 2021 to January 2023. The serum CaMKII, 5-hydroxytryptamine (5-HT), and brain-derived neurotrophic factor (BDNF) levels were measured by enzyme-linked immunosorbent assay method. Hamilton depression rating scale was used to assess the depression status of all study subjects. Hamilton anxiety rating scale, the self-rating anxiety scale, and the self-rating depression scale were used to further evaluate the psychological status of all patients. The self-rating depression scale, Hamilton anxiety rating scale, and self-rating anxiety scale scores in the depression group were significantly elevated compared to the non-depression group (P < .05). The serum CaMKII, 5-HT, and BDNF levels were significantly declined in the depression group compared to the non-depression group. Pearson analysis showed a positive correlation among CaMKII levels, 5-HT levels, and BDNF levels. Serum levels of CaMKII were associated with the psychological status of HVS patients (depression and anxiety). CaMKII could be used to predict depression in HVS patients. CaMKII was a risk factor for depression in HVS patients. This study showed that the serum CaMKII levels decreased in HVS patients with depression. The serum CaMKII level was correlated with 5-HT, BDNF and could be used to predict depression in HVS patients. Show less