Current Evidence and Future Directions of Berberine Intervention in Depression.

A major type of serious mood disorder, depression is currently a widespread and easily overlooked psychological illness. With the low side effects of natural products in the treatment of diseases becoming the pursuit of new antidepressants, natural Chinese medicine products have been paid more and more attention for their unique efficacy in improving depression. In a view from the current study, the positive antidepressant effects of berberine are encouraging. There is a lot of work that needs to be done to accurately elucidate the efficacy and mechanism of berberine in depression. In this review, the relevant literature reports on the treatment of depression and anxiety by berberine are updated, and the potential pharmacological mechanism of berberine in relieving depression has also been discussed.

Rapid anti-depressant-like effects of ketamine and other candidates: Molecular and cellular mechanisms.

Major depressive disorder takes at least 3 weeks for clinical anti-depressants, such as serotonin selective reuptake inhibitors, to take effect, and only one-third of patients remit. Ketamine, a kind of anaesthetic, can alleviate symptoms of major depressive disorder patients in a short time and is reported to be effective to treatment-resistant depression patients. The rapid and strong anti-depressant-like effects of ketamine cause wide concern. In addition to ketamine, caloric restriction and sleep deprivation also elicit similar rapid anti-depressant-like effects. However, mechanisms about the rapid anti-depressant-like effects remain unclear. Elucidating the mechanisms of rapid anti-depressant effects is the key to finding new therapeutic targets and developing therapeutic patterns. Therefore, in this review we summarize potential molecular and cellular mechanisms of rapid anti-depressant-like effects based on the pre-clinical and clinical evidence, trying to provide new insight into future therapy.

Role of leptin in the regulation of food intake in fasted mice.

Leptin is well acknowledged as an anorexigenic hormone that plays an important role in feeding control. Hypothalamic GABA system plays a significant role in leptin regulation on feeding and metabolism control. However, the pharmacological relationship of leptin and GABA receptor is still obscure. Therefore, we investigated the effect of leptin or combined with baclofen on the food intake in fasted mice. We detected the changes in hypothalamic c-Fos expression, hypothalamic TH, POMC and GAD67 expression, plasma insulin, POMC and GABA levels to demonstrate the mechanisms. We found that leptin inhibit fasting-induced increased food intake and activated hypothalamic neurons. The inhibitory effect on food intake induced by leptin in fasted mice can be reversed by pretreatment with baclofen. Baclofen reversed leptin's inhibition on c-Fos expression of PAMM in fasted mice. Therefore, these results indicate that leptin might inhibit fasting-triggered activation of PVN neurons via presynaptic GABA synaptic functions which might be partially blocked by pharmacological activating GABA-B. Our findings identify the role of leptin in the regulation of food intake.

Correction: The role of substance P in epilepsy and seizure disorders.

[This corrects the article DOI: 10.18632/oncotarget.20606.].

Stress-Induced Functional Alterations in Amygdala: Implications for Neuropsychiatric Diseases.

The amygdala plays a major role in the processing of physiologic and behavioral responses to stress and is characterized by gamma-aminobutyric acid (GABA)-mediated high inhibitory tone under resting state. Human and animal studies showed that stress lead to a hyperactivity of amygdala, which was accompanied by the removal of inhibitory control. However, the contribution of hyperactivity of amygdala to stress-induced neuropsychiatric diseases, such as anxiety and mood disorders, is still dubious. In this review, we will summarize stress-induced various structural and functional alterations in amygdala, including the GABA receptors expression, GABAergic transmission and synaptic plasticity. It may provide new insight on the neuropathologic and neurophysiological mechanisms of neuropsychiatric diseases.

The role of substance P in epilepsy and seizure disorders.

A range of evidence implicates the neuropeptide substance P (SP), a member of the tachykinin family, in emotional behavior, anxiety, pain, and inflammation. Recently, SP has been implicated in susceptibility to seizures, for which a potential proconvulsant role was indicated. Indeed, antagonists of a specific SP receptor, neurokinin-1 receptor, were found to attenuate kainic acid (KA)-induced seizure activity. However, detailed mechanisms of SP regulation in epilepsy remain obscure. In this review, we summarize the present literature to expound the role of SP in epilepsy, and provide hypotheses for potential mechanisms.