Tokumaru Osamu, Kitano Takaaki, Takei Hidehiro, Ogata Kazue, Kawazato Hiroaki, Yasuda Aiko, Nisimaru Naoko, Yokoi Isao
Department of Physiology, School of Medicine, Oita University Faculty of Medicine, Oita, Japan.
J Neurosurg. 2006 Dec;105 Suppl:202-7. doi: 10.3171/sup.2006.105.7.202.
Gamma Knife surgery (GKS) is performed to treat patients with functional neurological diseases, but the neurophysiological mechanisms of GKS's biological effects with subnecrotic doses remain largely undefined. The purpose of the present study was to investigate the effects of gamma irradiation on energy metabolism in the rat brain by using 31P nuclear magnetic resonance spectroscopy (31P-NMRS).
The whole brains of Wistar rats were irradiated with a subnecrotic (60-Gy) dose of radiation. One week after the irradiation, brain slices (400 microm thick) were incubated in standard artificial cerebrospinal fluid to undergo 31P-NMRS investigation. Changes in high-energy phosphate, phosphocreatine (PCr), and gamma-ATP, as well as inorganic phosphate levels before, during, and after ischemic stress for 64 minutes were measured. Histological findings were also evaluated using light and electron microscopy. The decrease in the PCr level was significantly slower during ischemia and recovery after reperfusion was significantly faster and greater in the gamma-irradiated rats than in the control animals. The gamma-ATP level after ischemia was also higher in the gamma-irradiated rats than in the controls. Neither neuronal damage nor astrocytosis was observed in the irradiated cerebral cortices.
Gamma irradiation with a subnecrotic dose may have neuroprotective effects that maintain a more stable cellular phosphorylation potential after ischemic stress. Such effects of GKS on energy metabolism coupled with neurotransmission (glutamate-glutamine cycling between neurons and astrocytes) may play a role in the treatment of neurological disease.
伽玛刀手术(GKS)用于治疗功能性神经疾病患者,但亚坏死剂量的GKS生物学效应的神经生理机制仍 largely 未明确。本研究的目的是通过使用 31P 核磁共振波谱(31P-NMRS)研究伽玛射线照射对大鼠脑能量代谢的影响。
用亚坏死剂量(60 Gy)的辐射照射 Wistar 大鼠的全脑。照射一周后,将脑片(400 微米厚)置于标准人工脑脊液中进行 31P-NMRS 研究。测量缺血应激 64 分钟前、期间和之后高能磷酸、磷酸肌酸(PCr)和γ-ATP 以及无机磷酸水平的变化。还使用光镜和电镜评估组织学结果。与对照动物相比,γ 射线照射的大鼠在缺血期间 PCr 水平的下降明显较慢,再灌注后恢复明显更快且更大。γ 射线照射的大鼠缺血后的γ-ATP 水平也高于对照组。在照射的大脑皮层中未观察到神经元损伤或星形细胞增生。
亚坏死剂量的伽玛射线照射可能具有神经保护作用,在缺血应激后维持更稳定的细胞磷酸化电位。GKS 对能量代谢以及神经传递(神经元和星形胶质细胞之间的谷氨酸-谷氨酰胺循环)的这种作用可能在神经疾病的治疗中起作用。