Potential sources of intrinsic optical signals imaged in live brain slices
Potential sources of intrinsic optical signals imaged in live brain slices
复制标题
DOI：
10.1006/meth.1999.0771
复制
发表时间：
1999-06-01
期刊：
影响因子：
--
通讯作者：
Obeidat, AS
中科院分区：
文献类型：
--
作者：
Andrew, RD;Jarvis, CR;Obeidat, AS
光在生物组织中如何被吸收或散射的变化被称为内在光学信号（IOS）。如果它涉及细胞内和细胞外隔室之间的显著水运动，则浸没的脑切片制备中的IOS成像提供了对脑活动的洞察。这包括对渗透压失衡、兴奋毒性谷氨酸激动剂和氧/葡萄糖剥夺的反应，后者导致扩散性抑郁。关于这些信号有几个误解。(1)IOS不是由胶质细胞肿胀单独产生的。虽然神经元和神经胶质源还不能直接成像，但几条证据表明神经元对透光率的变化有显着贡献。(2)兴奋毒性肿胀和渗透性肿胀在生理上是不同的，它们的相关IOS也是如此。低渗性肿胀不涉及皮质锥体神经元的可检测的神经元去极化，仅涉及从稀释介质中穿过细胞膜被动吸入水。相反，兴奋性毒性肿胀涉及与过量Na+和Cl-进入相关的持续膜去极化，随后是水，在后一种情况下，IOS表现出实质性损伤。(3)渗透扰动不诱导体积调节机制，如通过IOS测量的。在脑切片中通过IOS测量的渗透反应是被动的，没有在过度渗透应激下培养的脑细胞的研究所建议的规模上被假定为主动的补偿机制。（4）扩散性抑制（SD）可引起神经元损伤。在偏头痛先兆期间无害，SD诱导脑切片中的急性神经元损伤，所述脑切片由于氧/葡萄糖剥夺而代谢受损，如IOS所证实的，通过光透射率的最小降低来判断，SD不扩散的邻近组织保持相对健康。IOS显示，SD的代谢应激与能量资源的妥协相结合，导致对谷氨酸拮抗剂具有抗性的急性神经元损伤。(5)而高渗条件下减少ii引起细胞收缩，兴奋性毒性条件下减少LT引起树突状串珠。这种构象变化增加了光散射，即使组织继续膨胀。(C)北京：科学出版社.
Changes in how light is absorbed or scattered in biological tissue are termed intrinsic optical signals (IOSs), Imaging IOSs in the submerged brain slice preparation provides insight into brain activity if it involves significant water movement between intracellular and extracellular compartments. This includes responses to osmotic imbalance, excitotoxic glutamate agonists, and oxygen/glucose deprivation, the latter leading to spreading depression. There are several misconceptions regarding these signals. (1) IOSs are not generated by glial swelling alone. Although neuronal and glia sources cannot yet be directly imaged, several lines of evidence indicate that neurons contribute significantly to the changes in light transmittance. (2) Excitotoxic swelling and osmotic swelling are physiologically different, as are their associated IOSs. Hyposmotic swelling involves no detectable neuronal depolarization of cortical pyramidal neurons, only the passive drawing in of water from a dilute medium across the cell membrane, In contrast excitotoxic swelling involves sustained membrane depolarization associated with inordinate amounts of Na+ and Cl- entry followed by water, IOSs demonstrate substantial damage in the latter case. (3) Osmotic perturbations do not induce volume regulatory mechanisms as measured by IOSs. The osmotic responses measured by IOSs in brain slices are passive, without the compensatory mechanisms that are assumed to be active on a scale suggested by studies of cultured brain cells under excessive osmotic stress, (4) Spreading depression (SD) can cause neuronal damage, Innocuous during migraine aura, SD induces acute neuronal damage in brain slices that are metabolically compromised by oxygen/glucose deprivation, as demonstrated by IOSs, Neighboring tissue where SD does not spread remains relatively healthy as judged by a minimal reduction in light transmittance. IOSs show that the metabolic stress of SD combined with the compromise of energy resources leads to acute neuronal damage that is resistant to glutamate antagonists. (5) While hyperosmotic conditions reduce ii by causing cells to shrink, excitotoxic conditions reduce LT by causing dendritic beading. This conformational change increases light scattering even as the tissue continues to swell. (C) 1999 Academic Press.