Escitalopram or Novel Herbal Mixture Treatments during or following Exposure to Stress Reduce Anxiety-Like Behavior through Corticosterone and BDNF Modifications

Abstract

Anxiety disorders are a major public health concern worldwide. Studies indicate that repeated exposure to adverse experiences early in life can lead to anxiety disorders in adulthood. Current treatments for anxiety disorders are characterized by a low success rate and are associated with a wide variety of side effects. The aim of the present study was to evaluate the anxiolytic effects of a novel herbal treatment, in comparison to treatment with the selective serotonin reuptake inhibitor escitalopram. We recently demonstrated the anxiolytic effects of these treatments in BALB mice previously exposed to one week of stress. In the present study, ICR mice were exposed to post natal maternal separation and to 4 weeks of unpredictable chronic mild stress in adolescence, and treated during or following exposure to stress with the novel herbal treatment or with escitalopram. Anxiety-like behavior was evaluated in the elevated plus maze. Blood corticosterone levels were evaluated using radioimmunoassay. Brain derived neurotrophic factor levels in the hippocampus were evaluated using enzyme-linked immunosorbent assay. We found that (1) exposure to stress in childhood and adolescence increased anxiety-like behavior in adulthood; (2) the herbal treatment reduced anxiety-like behavior, both when treated during or following exposure to stress; (3) blood corticosterone levels were reduced following treatment with the herbal treatment or escitalopram, when treated during or following exposure to stress; (4) brain derived neurotrophic factor levels in the hippocampus of mice treated with the herbal treatment or escitalopram were increased, when treated either during or following exposure to stress. This study expands our previous findings and further points to the proposed herbal compound's potential to be highly efficacious in treating anxiety disorders in humans.

The protective role of musk on salivary glands of mice exposed to chronic unpredictable mild stress

“…The mice were weighed before the start and after finishing the experiment. They were divided into 4 groups: an untreated control group (n = 10) and three other groups (n = 10 each) exposed to CUMS for 4 weeks, as described by Doro et al (13). The latter three groups were exposed, respectively, to CUMS plus 5% amyl acetate (CUMS group), CUMS and FLU (CUMS+FLU group) and CUMS and musk (CUMS+M group).…”

Neuroadaptations of the 5-HT System Induced by Antidepressant Treatments: Old and New Strategies

“…A very recent study reported that long-term administration of the SSRI escitalopram to mice, experiencing postnatal maternal separation plus 4 weeks of UCMS in adolescence, induced an elevation of BDNF levels in the hippocampus [114]. This result was obtained when stressed mice were treated either during or following exposure to stress, demonstrating that antidepressants are capable of blocking and reversing the negative effect of stress via BDNF actions [114]. Such modulation of BDNF concentrations seemed to be time-dependent.…”

“…Indeed, it has been reported that chronic treatment with different classes of antidepressants (SSRIs fluoxetine and escitalopram, MAOIs tranylcypromine and phenelzine, TCA desipramine) increases BDNF brain levels [101,[110][111][112][113]. A very recent study reported that long-term administration of the SSRI escitalopram to mice, experiencing postnatal maternal separation plus 4 weeks of UCMS in adolescence, induced an elevation of BDNF levels in the hippocampus [114]. This result was obtained when stressed mice were treated either during or following exposure to stress, demonstrating that antidepressants are capable of blocking and reversing the negative effect of stress via BDNF actions [114].…”

Histological and molecular techniques utilized to investigate animal models of depression. An updated review

“…It was reported that CUS‐induced depression significantly decreased BDNF protein levels (Ali et al., ; Banerjee et al, ; Li et al, ; Mao et al, ; Yu et al, ) in the hippocampus and frontal cortex as compared with the controls. For the determination of GR and BDNF protein level either Western blot analysis (Li et al, 2013a,b; Wang et al, ) or sandwich enzyme‐linked immunosorbent assay (ELISA) (Ali et al, Ayuob et al, ; Doron et al, ) was utilized (see Figure ).…”