Morphological and functional changes in visual cortex after retinal damage and its pharmacological approach

我们用正电子发射断层扫描(PET)检测了实验性高血压性青光眼继发的外侧膝状核(LGN)变性作为青光眼的指标，并通过形态学和免疫组织化学检查证实了胶质细胞的激活。此外，我们还研究了内质网(ER)应激是否参与了高眼压后LGN神经元死亡的病理生理机制。在本研究中，我们认为内质网应激可能在高眼压后LGN神经元死亡中起关键作用，胶质细胞激活发生在LGN，单眼高眼压后的PET成像可以检测到LGN的变性。因此，激活的神经胶质标记物，如LGN中的PBR，可能在青光眼的无创分子成像诊断中有用。

We examined lateral geniculate nucleus(LGN) degeneration secondary to experimental hypertensive glaucoma as an indicator for glaucoma in ocular hypertensive monkeys using positron emission tomography(PET), and validated glial activation by morphological and immunohistochemical examinations. Furthermore, we investigated whether endoplasmic reticulum(ER) stress was involved in the pathophysiological mechanisms underlying neuronal death of the LGN after intraocular pressure(IOP) elevation. In the present study, we showed that ER stress may play a pivotal role in neuronal death of the LGN after IOP elevation, that glial activation occurs in the LGN, and that the LGN degeneration could be detected by a PET imaging after unilateral ocular hypertension. Therefore, activated glial markers such as PBR in the LGN may be useful in noninvasive molecular imaging for diagnosis of glaucoma.