Abstract
Tetragonia tetragonioides, which is a halophyte and grows widely in Asian-Pacific regions, has been used for the treatment of digestive disorders in traditional oriental medicine. This study examined the potential antidepressant effect of Tetragonia tetragonioides in an astroglial degeneration model of depression, which was established based on the postmortem study of depressive patients' brain presenting diminished astrocytes in the prefrontal cortex. C57BL/6 male mice were exposed to glial ablation in the prefrontal cortex by the administration of the gliotoxin, L-alpha-aminoadipic acid (L-AAA) to induce depression. Tetragonia tetragonioides at doses of 100 mg/kg and 300 mg/kg, imipramine at a dose of 15 mg/kg, and distilled water were orally administrated to mice for 18 days. Behavioral tests including the open field test (OFT), sucrose preference test (SPT), forced swimming test (FST), and tail suspension test (TST) were carried out after 2 days of L-AAA injection. The expression levels of GFAP and NeuN in the prefrontal cortex were determined by immunohistochemistry. Mice subjected to glial ablation in the prefrontal cortex displayed decreased sucrose consumption in SPT and increased immobility time in FST and TST. Treatment with imipramine and Tetragonia tetragonioides remarkably ameliorated the behavioral despair induced by L-AAA. In addition, immunohistochemistry analysis showed that treatment with Tetragonia tetragonioides significantly restored the glial loss as indicated by the elevated GFAP expression level. These findings suggest that Tetragonia tetragonioides exerts an antidepressant effect through the restoration of glial loss under conditions of depression and can be a candidate for an antidepressant agent.
Highlights
A depressive disorder is identified as characteristic symptoms of despair, anhedonia, loss of appetite or sleep disturbance, decreased energy and concentration, and feeling of guilt and worthlessness [1,2,3,4,5]
Abnormalities in glial cells, especially astrocytes, play an important role in mediating major depressive disorders. e previous review summarized that the expression of the glial fibrillary acidic protein (GFAP) and representative astrocyte related proteins was significantly decreased in subjects with major
Based on the postmortem research studies reporting a loss of glia in prefrontal and the cingulate area from depressed patients [17], Banasr and Duman proved that glial ablation in the prefrontal cortex induced depressive-like behaviors [18]. e authors provoked the astrocytic degeneration by infusing L-alpha-aminoadipic acid (L-AAA), a gliotoxin specific for astrocytes [19], into prefrontal cortex
Summary
A depressive disorder is identified as characteristic symptoms of despair, anhedonia, loss of appetite or sleep disturbance, decreased energy and concentration, and feeling of guilt and worthlessness [1,2,3,4,5]. Chronic and acute stress induced depressive-like symptoms in behavior and alterations in astrocytes in the brain [15]. Based on the postmortem research studies reporting a loss of glia in prefrontal and the cingulate area from depressed patients [17], Banasr and Duman proved that glial ablation in the prefrontal cortex induced depressive-like behaviors [18]. E antidepressant effect of TTK in the depressive models has not been tested, and previous studies indicated the possibility that TTK may be effective on treating depressive disorders. To address this topic, a depression model of astroglial degeneration was used to investigate the ameliorative effects of TTK on depressive symptoms. We examined the possible mechanism behind the antidepressant-like effects of TTK by examining the expression of the GFAP in the prefrontal region in mice brain
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
