Accumulating evidence shows that patients with neurological and psychiatric disorders are often associated with gut microbiota disorders. Our previous work using rodent model demonstrated …show more content…
We inferred, however, that reducing the intestinal epithelium permeability by strengthening the tight junction may have a facilitating effect on decreasing peripheral levels of LPS and pro-inflammatory cytokines, but would fail to elicit beneficial effects on neuropsychiatric diseases. Inflammation is thought to influence brain function at a higher level, and elicits a constellation of symptoms, designated as 'sickness behaviour'. There is evidence that the brain has physiological potential to recognize inflammatory cytokines as a molecular signal for sickness behavior. LPS, a cytokine producer, is capable to induce all nonspecific sickness symptoms, including fever, activation of the hypothalamic-pituitary-adrenal (HPA) axis, food intake reduction and other abnormally behavioral activities. Bases on these findings, we therefore think that sickness behavior is completely different from neuropsychiatric diseases, particularly depression. Inhibiting activated inflammatory response might help to relieve the sickness symptoms. However, for neuropsychiatric disorders, in addition to therapeutic strategy targeting anti-inflammatory responses, improving the level of monoamine neurotransmitters is more of …show more content…
Interestingly, depression patients are often accompanied by physical symptoms, in which the intestinal symptoms are more common. In addition to anti-cholinergic drugs, antidepressants and/or anxiolytics are similarly effective in therapeutic effects on IBS. It is has been widely known that the intestine is a major place for the synthesis of monoamine neurotransmitters, especially serotonin. Although enterochromaffin cells (ECs) accounted for less than 1% of intestinal epithelial cells, 95% of serotonin in the human body is produced and released form ECs. The pathogenesis of depression is mainly due to the lack of 5-tryptophan (5-HT) in the synaptic cleft. Currently, conventional antidepressant agents are designed to increase 5-HT via inhibiting 5-HT reuptake. Although there is no direct evidence that the onset of antidepressants is dependent on stimulating 5-HT release in ECs, we think that ECs, at least partially, play a critical role in the process of depression