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Decreased Expression of NHE1 in Lithium Treated Rat Hippocampus
김중모,정용욱 동국대학교 의학연구소 2008 東國醫學 Vol.15 No.1
인간과 흰쥐에서 lithium의 장기적 복용은 온몸과 대뇌의 대사성산증을 초래하며 이는 H^(+)의 분비감소 혹은 HCO₃^(-)의 흡수증가에 기인한 것으로 생각된다. 그러나 낮은 농도에서의 lithium의 장기적투여가 뇌에서의 산 염기의 이상에 예민하게 반응하는 해마의 산-염기 운반자 단백질의 발현에 영향을 미치는가의 여부는 알려져 있지 않다. Lithium의 처치는 25일간 쥐 분말사료에 lithium 60 mmol/dl를 투여하였다. 혈장에서 lithium의 농도는 임상적으로 이용되는 치료농도의 범주에 해당하는 0.76 ± 0.2mEq/L으로 대조군에 비하여 증가하였다. Lithium처리 된 흰쥐에서 산 염기조절단백질인 Na^(+)/H^(+) exchanger isoform 1 (NHE1) 와 electrogenic Na^(+)/HCO₃^(-) cotransporter (eNBC) 의 발현변화는 흰쥐해마에서 조사하였다. Lithium처리 후 NHE1의 발현은 37 ± 8% (n=8, p<0.01)로 대조군에 비해 통계학적으로 의미있게 감소하였으나 eNBC의 발현에는 변화가 없었다. 이러한 결과들은 lithium의 장기적 투여가 해마내 산 염기조절운반자의 발현을 의미있게 변화시킬 수 있음을 의미한다. 이것은 흰쥐 해마에서 H^(+)의 분비를 감소하여 대사성산증을 방지하려는 직접적 혹은 보상적 효과의 하나로 생각된다. Prolonged lithium treatment of humans and rodents often results in systemic and cerebral metabolic acidosis. This is thought to be caused by diminished net H^(+) secretion and/or increased net uptake of bicarbonate. However, it is unclear that chronic treatment with lithium at a low dose is associated with changes in the expression of brain acid-base transporters in the hippocampus which is well known to response to brain acid-base imbalance. Chronic lithium treatment was produced by pellet of standard diet containing 60mmol /dl lithium citrate for 25 days. The serum concentrations of lithium were increased to 0.76 ± 0.2 mEq/L which is therapeutic dose of clinical practice. The changes of protein expression of acid-base transporters [Na^(+)/H^(+) exchanger isoform 1 (NHE1) and electrogenic Na^(+)HCO₃^(-) cotransporter (eNBC)] were examined in the lithium treated rat hippocampus. Immunoblott analyses revealed that the expression of NHE1 (37 ± 8% of controls, n=8, P<0.01) was significantly decreased. In contrast, the expression of eNBC was unchanged in lithium treated rat hippocampus compared with that of controls. These results demonstrate that the expression of hippocampus acid base transporter is markedly altered in response to long term lithium treatment. This is likely to represent direct or compensatory effects to decrease the H^(+) secretion to prevent the development of metabolic acidosis in the hippocampus.
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Altered Expression of eNOS and VEGF in the Rat Choroid Plexus following Systemic Hyponatremia
김중모,정용욱 대한해부학회 2008 Anatomy & Cell Biology Vol.41 No.3
In the present study, alterations of the endothelial nitric oxide synthase (eNOS) and the vascular endothelial growth factor (VEGF) expression in the third ventricle choroid plexus and their effects to the adjacent hippocampus were studied in the systemic hyponatremic model with the total of 29 adult male Spraque-Dawley rats. Systemic hyponatremia was induced by the coadministration of 30mL(~12% body weight) dextrose solution (140 mmol/L) intraperitoneally and a 3-μg subcutaneous dose of 1-deamino-8-D-arginine vasopressin (dDAVP). Two and six hours after the drug administration, there were significant reductions in the serum osmolarity (252±5.1 and 252±6.4 mOsm /L) and in Na+ concentration (117±1.7 and 97.2 mM) from the control values (osmolarity: 296±5.2 mOsm/L, Na+ concentration: 140±4.7 mM). The expression levels of eNOS and VEGF protein in the choroid plexus were determined by using immunohistochemistry and quantitative immunoblotting. There was a significant increase in the expression of the eNOS (135%±2%, P⁄0.05), whereas the expression of the VEGF was slightly increased compared with the control rats after 2 h of systemic hyponatremia. 6 h after the onset of systemic hyponatremia, expression of the eNOS and the VEGF was decreased simultaneously. Consistent with the expression of the eNOS in choroid plexus after 2 h after systemic hyponatremia, cresyl violet staining revealed necrotic cell death in the hippocampus CA3 subfield, presumably resulting from cerebrospinal fluid (CSF) overproduction and subsequent an elevation of intracranial pressure. Thus, activation of the eNOS protein in the choroid plexus may be one of the molecular mechanisms of the hippocampal cell injury. Additionally, substantial decrease of eNOS and VEGF expression in the choroid plexus after 6 h of the systemic hyponatremia may reflect the eNOS and VEGF in response to the systemic hyponatremia undergo the regulatory changes to prevent the overproduction of CSF. Overall, these results suggest that NO-mediated excessive water influx into the ventricle is important for the cerebral pathogenesis after the systemic hyponatremia.
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