4.4 Article

Glatiramer acetate attenuates depressive/anxiety-like behaviors and cognitive deficits induced by post-weaning social isolation in male mice

Journal

PSYCHOPHARMACOLOGY
Volume 238, Issue 8, Pages 2121-2132

Publisher

SPRINGER
DOI: 10.1007/s00213-021-05836-5

Keywords

MDD; Glatiramer acetate; Behavioral tests; Social isolation; BDNF

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The study investigated the antidepressant potential of glatiramer acetate in male mice using acute and chronic models of depression. The results showed that GA improved depressive-/anxiety-like behaviors and cognitive dysfunction, with effects on BDNF levels.
Rationale Major depressive disorder (MDD) is a debilitating disorder with adverse effects on mood, memory, and quality of life. Objectives In this study, the antidepressant potential of glatiramer acetate (GA), a drug used in the management of multiple sclerosis, was investigated in acute and chronic models of depression in male mice. The acute antidepressant screening was performed with the forced swim (FST) and tail suspension (TST) tests. In the chronic phase, post-weaning social isolation (SI) was used to induce depressive-/anxiety-like behaviors. Methods Mice were reared in two different groups of social (SG) and isolated (IG) for 4 weeks. IG mice were treated with 0.5, 1.0, and 2.0 mg/kg of GA for the last 2 weeks of the SI period. Animals were assessed by the behavioral tests of depression, anxiety, learning, and memory, and hippocampal brain-derived neurotrophic factor (BDNF) level was measured. Results The acute tests confirmed the antidepressant potential of GA. In the chronic phase, GA could reduce immobility time in FST (P < 0.05), increase exploration activity in open field test (P < 0.05), increase open arms duration (P < 0.05) and entries in elevated plus maze (P<0.001), and improve memory and learning in passive avoidance test (P < 0.05). The BDNF level was increased in IG mice and decreased in IG mice treated with GA. Conclusions Our results showed that GA improved depressive-/anxiety-like behaviors and cognitive dysfunction of SI reared mice without increasing the BDNF level which may be associated with other mechanisms of actions of GA.

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