Inflammation as the Potential Basis in Depression / 대한배뇨장애요실금학회지

There is growing evidence of the association between inflammation and stress-related disorders including depression. The positive correlation between the increased levels of inflammatory cytokines observed in patients with other diseases and the byproduct of the depressive symptoms may be caused by chronic stress. Increased neuroinflammatory responses are capable of activating microglia and astrocytes, which leads to release pro-inflammatory cytokines. Moreover, elevated levels of inflammatory cytokines such as tumor necrosis factor-alpha, interleukin (IL)-1, and IL-6 are causally related to various aspects of depression such as the behavioral symptomatology. Eventually, these elevated cytokines aggravate and propagate neuroinflammation, impairing brain functions. Thus, activated astrocytes and microglia may be potential mediators in neuroinflammatory processes contributing to the development of depression.

Long-term Treatment with Oriental Medicinal Herb Artemisia princeps Alters Neuroplasticity in a Rat Model of Ovarian Hormone Deficiency

Artemisia princeps (AP) is a flowering perennial used as a traditional medicine and dietary supplement across East Asia. No study has yet assessed its effects on synaptic plasticity in hippocampus and much less in a model of ovarian hormone deficiency. We examined the influence of chronic oral AP ethanol extract treatment in ovariectomized rats on the induction of long-term depression in a representative synapse (CA3-CA1) of the hippocampus. Ovariectomized rats demonstrated lower trabecular mean bone mineral densities than sham, validating the establishment of pathology. Against this background of pathology, AP-treated ovariectomized rats exhibited attenuated long-term depression (LTD) in CA1 relative to water-treated controls as measured by increased field excitatory post-synaptic potentials (fEPSP) activation averages over the post-stimulation period. While pathological significance of long-term depression (LTD) in ovariectomized rats is conflicting, that AP treatment significantly affected its induction offers justification for further study of its influences on plasticity and its related disorders.

Study of dopamine transporter in the rat 6-hydroxydopamine Parkinson's disease model

BACKGROUND: Neuroprotective therapy is essential in the management of Parkinson's disease(PD). As symptomatic benefit of a treatment may clinically mask the disease progression, an evaluation of the effect of a neuroprotective therapy should be based on objective measurement of in vivo dopaminergic integrity: Nuclear imaging techniques such as SPECT or PET can visualize dopaminergic system using dopamine transporter ligands and show the promise for this purpose. The objective of this study is to examine the changes of dopamine transporter in the animal model of PD and those correlations with behavioral and biochemical changes. METHODS: We injected 6-hydroxydopamine into the substantia nigra in Sprague-Dawley rats to establish the unilateral PD model, and examined the rotation response after apomorphine injection as a behavioral aspect of the animal model. And we also measured the dopamine and DOPAC level in the striata and the dopamine transporter by [3H]-mazindol autoradiography. RESULTS: We observed that the rats showed turning behavior only after severe reduction of dopamine and DOPAC. There was a strong inverse correlation between rotation behavior and striatal dopamine, DOPAC and dopamine transporter density. There was a positive and strong linear-correlation between dopamine transporter density and dopamine or DOPAC levels. CONCLUSION: Measurement of dopamine transporter gives a good estimate of striatal dopamine level in an animal model of PD. In vivo measurement of dopamine transporter will give an objective information on the integrity of presynaptic nigrostriatal dopaminergic system.