Abstract
Backgroud: Chronic restraint stress (CRS) induces depressive-like behaviors in rodents, which involves dysregulation of hippocampal synapse formation and excessive autophagy. Adiponectin has antidepressant activity. Hydrogen sulfide (H2S) is a novel gasotransmitter. The present work was to investigate whether H2S antagonizes CRS-induced depressive-like behaviors in rats and to explore whether its potential mechanism involves ameliorated synaptic and autophagic dysregulation by upregulation of adiponectin.Methods: Depressive-like behavior was analyzed by the tail suspension test (TST), novelty suppressed feeding test (NSFT), and open field test (OFT). The structure of autophagy was observed under transmission electron microscopy. The expressions of adiponectin, beclin1, and sequestosome 1 (p62/SQSTMI) protein in hippocampus were measured by Western blot. The levels of synapsin1 (SYN1) in the hippocampus were calculated by Western blot and immunofluorescence technique.Results: The behavior experiments, including TST, NSFT, and OFT, showed that NaHS (a donor of H2S) reduced CRS-induced depressive-like behaviors. NaHS decreased the loss of hippocampal synapse as evidenced by increased the level of SYN1 in the hippocampus of CRS-exposed rats. NaHS rescued CRS-induced excessive hippocampal autophagy as evidenced by declines in the number of autophagosomes and the expression of beclin1 as well as increase in the expression of P62 in the hippocampus of CRS-exposed rats. NaHS upregulated hippocampal adiponectin expression in the CRS-exposed rats. Furthermore, neutralizing adiponectin by Anti-acrp30 reversed the protective response of NaHS to CRS-produced depressive-like behaviors as well as hippocampal synaptic disruption and excessive autophagy.Conclusion: H2S mitigates CRS-induced depressive behavior via upregulation of adiponectin, which in turn results in amelioration in hippocampal synapse formation dysfunction and excessive autophagy.
Highlights
Depression is a kind of serious mental disease that was caused by a variety of reasons
It has been reported that chronic restraint stress (CRS) leads to neurological changes and depressive-like behaviors of rodents [3], which is widely applied in animal experiments to study the etiology and pathophysiology of depression [4,5,6]
In novelty suppressed feeding test (NSFT), the latency to feed in CRS-exposed rats was obviously decreased after administration of NaHS, while NaHS alone didn’t change it in normal rats (Figure 2C)
Summary
Depression is a kind of serious mental disease that was caused by a variety of reasons. Chronic stress is considered as a triggering factor in the pathogenesis of depression [1, 2]. It has been reported that chronic restraint stress (CRS) leads to neurological changes and depressive-like behaviors of rodents [3], which is widely applied in animal experiments to study the etiology and pathophysiology of depression [4,5,6]. Hydrogen sulfide (H2S) is recognized as a neuroprotectant, which plays important roles in the central nervous system (CNS) [7]. Our team verified that administration of H2S antagonizes depressive-like behaviors in streptozotocin-exerted diabetic rats [8]. We will further explore whether H2S has bioavailability to prevent CRSinduced depressive-like behaviors
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