Gerashchenko Dmitry, Murillo-Rodriguez Eric, Lin Ling, Xu Man, Hallett Laura, Nishino Seiji, Mignot Emmanuel, Shiromani Priyattam J
West Roxbury VA Medical Center and Harvard Medical School, West Roxbury, MA 02132, USA.
Exp Neurol. 2003 Dec;184(2):1010-6. doi: 10.1016/S0014-4886(03)00388-1.
The sleep disorder narcolepsy may now be considered a neurodegenerative disease, as there is a massive reduction in the number of neurons containing the neuropeptide, hypocretin (HCRT). Most narcoleptic patients have low to negligible levels of HCRT in the cerebrospinal fluid (CSF), and such measurements serve as an important diagnostic tool. However, the relationship between HCRT neurons and HCRT levels in CSF in human narcoleptics is not known and cannot be directly assessed. To identify this relationship in the present study, the neurotoxin, hypocretin-2-saporin (HCRT2-SAP), was administered to the lateral hypothalamus (LH) to lesion HCRT neurons. CSF was extracted at circadian times (ZT) 0 (time of lights-on) or ZT8 at various intervals (2, 4, 6, 12, 21, 36, 60 days) after neurotoxin administration. Compared to animals given saline in the LH, rats with an average loss of 73% of HCRT neurons had a 50% decline in CSF HCRT levels on day 60. The decline in HCRT levels was evident by day 6 and there was no recovery or further decrease. The decline in HCRT was correlated with increased REM sleep. Lesioned rats that were kept awake for 6 h were not able to release HCRT to match the output of saline rats. As most human narcoleptics have more than 80% reduction of CSF HCRT, the results from this study lead us to conclude that in these patients, virtually all of the HCRT neurons might be lost. In those narcoleptics where CSF levels are within the normal range, it is possible that not all of the HCRT neurons are lost and that the surviving HCRT neurons might be increasing output of CSF HCRT.
睡眠障碍发作性睡病现在可能被视为一种神经退行性疾病,因为含有神经肽下丘脑分泌素(HCRT)的神经元数量大幅减少。大多数发作性睡病患者脑脊液(CSF)中的HCRT水平很低或可忽略不计,此类测量是一项重要的诊断工具。然而,人类发作性睡病患者中HCRT神经元与脑脊液中HCRT水平之间的关系尚不清楚,也无法直接评估。为了在本研究中确定这种关系,将神经毒素下丘脑分泌素-2-皂草素(HCRT2-SAP)注入外侧下丘脑(LH)以损伤HCRT神经元。在注入神经毒素后的不同时间间隔(2、4、6、12、21、36、60天)的昼夜时间(ZT)0(开灯时间)或ZT8采集脑脊液。与在LH中注射生理盐水的动物相比,平均损失73%的HCRT神经元的大鼠在第60天时脑脊液HCRT水平下降了50%。HCRT水平在第6天就明显下降,且没有恢复或进一步下降。HCRT的下降与快速眼动睡眠增加相关。保持清醒6小时的损伤大鼠无法释放HCRT以匹配注射生理盐水大鼠的输出。由于大多数人类发作性睡病患者脑脊液HCRT减少超过80%,本研究结果使我们得出结论,在这些患者中,几乎所有的HCRT神经元可能都已丧失。在那些脑脊液水平处于正常范围内的发作性睡病患者中,有可能并非所有的HCRT神经元都已丧失,且存活的HCRT神经元可能在增加脑脊液HCRT的输出。