• 생물정신의학
• /
• 제8권2호
• /
• pp.220-225
• /
• 2001

As numbers of serotonin's function are so many, studies of serotonin are numerous nowadays. In the beginning, concentration of metabolites such as 5-HIAA was a key issue, but recent studies have been challenged for serotonin receptor genes and their relation to mood disoder. Serotonin transporter(5-HTT) gene is a strong candidate gene of mood disoder for following reason. Serotonin transporter is a key protein in the serotonin pathway as it regulate the concentration of serotonin in the synaptic clept and essential pathophysiology of depression is dysregulation of 5-HTT so that all antidepressants have effect of 5-HTT antagonist. The decrease of 5-HTT in the platelet and in brain of the depressive patients is much consistent results in the studies of the pathophysiology of mood disorder till now. By this, we will be able to develop simple and easy marker for diagnosis, type, and treatment monitoring of depression. Many psychiatrists have sought the independent genes in relation to depression or schizophrenia. Obviously, the hereditary vulnerability contributes to etiology of mood disorders, but it is difficult to discriminate the independent genes because of many environmental factors. Moreover, in the hereditarily complex diseases such as mood disorder, the only vulnerability of gene can not sufficiently explain the etiology. In the future, to exclude the role of the gene-environmental interaction, the methods such as gene transfer can be considered. In the opposite direction, by using the gene destruction method, the role of target genes can be examined. As yet the concept of the gene expression, neural plasticity, neurogenesis and etc, is the elementary stage. The development of this field will help to establish the treatment strategy of chronic and refractory mood disorders.

• 동의생리병리학회지
• /
• 제18권4호
• /
• pp.1041-1054
• /
• 2004

Electroacupuncture (EA) has been reported to increase pain threshold, and to enhance the NK cell activity by up-regulation of IFN-γ and endogenous β-endolphin. For the purpose of understanding the molecular mechanism of EA stimulation, we analyzed the gene expression profile of rat hypothalamus, treated on Zusanli (ST36) with EA, in comparison with control group by oligonucleotide chip microarray (Affymetrix GeneChip Rat Neurobiology U34 Array) and real-time RT-PCR. Sprague-Dawley (S-D) male rats were stimulated at the Zusanli (ST36) acupoint in restriction holder. Simultaneously the control group was given only holder stress without EA stimulation. In order to prove the appropriateness of EA treatment, we measured spleen NK cell activity with standard 51Cr release assay. NK cell activity of EA group was significantly increased comparing to control group. The microarray and PCR results show that EA treatment up-regulates expression of genes associated with 1) nerve growth such as NGF induced factor A and VGF, 2) signal transduction such as 5HT3 receptor subunit, AMPA receptor binding protein and Na-dependent neurotransmitter transporter, and 3) anti-oxidation such as superoxide dismutase and glutathione S-transferase. In addition, the activity of the anti-oxidative enzyme, SOD of hypothalamus, liver and RBC was enhanced compared to that of control. The list of differentially expressed genes may implicate further insight on the mechanism of acupuncture effects.