Fujisawa Haruki, Sugimura Yoshihisa, Takagi Hiroshi, Mizoguchi Hiroyuki, Takeuchi Hideyuki, Izumida Hisakazu, Nakashima Kohtaro, Ochiai Hiroshi, Takeuchi Seiji, Kiyota Atsushi, Fukumoto Kazuya, Iwama Shintaro, Takagishi Yoshiko, Hayashi Yoshitaka, Arima Hiroshi, Komatsu Yukio, Murata Yoshiharu, Oiso Yutaka
Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Nagoya, Japan;
Futuristic Environmental Simulation Center, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan;
J Am Soc Nephrol. 2016 Mar;27(3):766-80. doi: 10.1681/ASN.2014121196. Epub 2015 Sep 16.
Hyponatremia is the most common clinical electrolyte disorder. Once thought to be asymptomatic in response to adaptation by the brain, recent evidence suggests that chronic hyponatremia may be linked to attention deficits, gait disturbances, risk of falls, and cognitive impairments. Such neurologic defects are associated with a reduction in quality of life and may be a significant cause of mortality. However, because underlying diseases such as adrenal insufficiency, heart failure, liver cirrhosis, and cancer may also affect brain function, the contribution of hyponatremia alone to neurologic manifestations and the underlying mechanisms remain unclear. Using a syndrome of inappropriate secretion of antidiuretic hormone rat model, we show here that sustained reduction of serum sodium ion concentration induced gait disturbances; facilitated the extinction of a contextual fear memory; caused cognitive impairment in a novel object recognition test; and impaired long-term potentiation at hippocampal CA3-CA1 synapses. In vivo microdialysis revealed an elevated extracellular glutamate concentration in the hippocampus of chronically hyponatremic rats. A sustained low extracellular sodium ion concentration also decreased glutamate uptake by primary astrocyte cultures, suggesting an underlying mechanism of impaired long-term potentiation. Furthermore, gait and memory performances of corrected hyponatremic rats were equivalent to those of control rats. Thus, these results suggest chronic hyponatremia in humans may cause gait disturbance and cognitive impairment, but these abnormalities are reversible and careful correction of this condition may improve quality of life and reduce mortality.
低钠血症是最常见的临床电解质紊乱。曾经认为大脑适应后低钠血症无症状,但最近的证据表明,慢性低钠血症可能与注意力缺陷、步态障碍、跌倒风险和认知障碍有关。这些神经缺陷与生活质量下降相关,可能是死亡的重要原因。然而,由于肾上腺功能不全、心力衰竭、肝硬化和癌症等基础疾病也可能影响脑功能,仅低钠血症对神经表现的贡献及其潜在机制仍不清楚。利用抗利尿激素分泌不当综合征大鼠模型,我们在此表明,血清钠离子浓度持续降低会导致步态障碍;促进情境恐惧记忆的消退;在新物体识别测试中导致认知障碍;并损害海马CA3-CA1突触的长时程增强。体内微透析显示,慢性低钠血症大鼠海马中的细胞外谷氨酸浓度升高。持续的低细胞外钠离子浓度也会降低原代星形胶质细胞培养物对谷氨酸的摄取,提示长时程增强受损的潜在机制。此外,纠正低钠血症大鼠的步态和记忆表现与对照大鼠相当。因此,这些结果表明,人类慢性低钠血症可能导致步态障碍和认知障碍,但这些异常是可逆的,谨慎纠正这种情况可能会改善生活质量并降低死亡率。