Abstract
Previous studies have shown the therapeutic properties of ginseng and ginsenosides on hyperactive and impulsive behaviors in several psychiatric diseases. Herein, we investigated the effect of Panax ginseng Meyer (PG) on hyperactive/impulsive behaviors in a manic-like animal model, sleep deprivation (SD) rats. Male rats were sleep-deprived for 48 h, and PG (200 mg/kg) was administered for 4 days, from 2 days prior to the start of SD to the end date of SD. The elevated plus maze (EPM) test showed that PG alleviated the increased frequency of entries into and spent time within open arms by SD. In order to investigate the molecular mechanism on this effect of PG, we assessed differentially expressed genes (DEGs) in the prefrontal cortex of PG-treated SD rats using RNA sequencing (RNA-seq) and performed gene-enrichment analysis for DEGs. The gene-enrichment analysis showed that PG most prominently affected the glutamatergic synapse pathway. Among the glutamatergic synapse pathway genes, particularly, PG enhanced the expressions of glutamate transporter Slc1a3 and Slc1a2 reduced in SD rats. Moreover, we found that PG could inhibit the SD-induced phosphorylation of the NR2A subunit of the NMDA receptor. These results suggested that PG might have a therapeutic effect against the manic-like behaviors, regulating the glutamatergic neurotransmission.
Highlights
Sleep disturbance is the most frequent symptom in manic episodes and a relapse factor of manic episodes in bipolar disorder (BPD) [1, 2]
The effect of Panax ginseng Meyer (PG) on the hyperactive- and impulsive-like behaviors was assessed in sleep deprivation (SD) rats using the elevated plus maze (EPM) test
The frequency of the total entries to the open and close was increased in SD rats compared to control rats, whereas PG-treated SD rats revealed a lower frequency of total entries than SD rats (Figure 1(c))
Summary
Sleep disturbance is the most frequent symptom in manic episodes and a relapse factor of manic episodes in bipolar disorder (BPD) [1, 2]. In rats and mice, SD rodents have shown maniclike behaviors, including locomotor hyperactivity, hypersexuality, irritability, and aggressiveness, as observed during the manic phase in patients with BPD [3, 4]. Treatments of mood stabilizers such as lithium and valproic acid, which are have been used for relieving in the manic episodes in BPD, reduced these manic-like behaviors in SD animals [5,6,7]. Neurochemical alterations in SD animals were represented, similar to patients during the manic phase in BPD. In the brains of SD animals, the dopaminergic hyperactivity, the increased activity of protein kinase C, and the decreased levels of brain-derived neurotrophic factor (BDNF) were observed [5, 8,9,10]
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