The Establishment Of Chronic Experimental Glaucoma Rats Model And Expression Of The Nogo, NgR In Retina Of The Models

BackgroundAs fact as we know that intraocular hypertension is the major risk factor for glaucomatous optic neuropathy.Retina and optic nerve are target organs of glaucoma damage. Pathological mechanism of glaucomatous optic neuropathy is progressive death of retina ganglion cells (RGCs) and optic nerve fiber degeneration, which leads to irreversible damage.Lots of studies have shown that why the damage caused by the primary insult is propagated rapidly and irreversibly beyond the initial lesion, and multitude factors participate in glaucomatous occurrence and development. Substantial progress has been made in understanding why the injured central nervous system (CNS) fails to regenerate. Nogo and NgR could been a reason of those in the glaucoma.Nogo, is a member of the reticulon family of membrane-associated molecules, Three different transcripts(A,B,C)were originally described as being formed from the gene, coding for three proteins: NogoA,NogoB, and NogoC,It was considered that Nogo66, the common to all three forms,inhibits axonal extension and induces the collase of growthcones. After CNS injury, NgR has been identified as a putative Nogo-66 receptor.This molecule binds Nogo66 with high affinity and its expression has been shown to be sufficient to confer sensitivity to Nogo66 on otherwise insensitive cells. And if Nogo66 is a major factor/molecule responsible for the failure of axonal regeneration in the CNS, and then the finding the expression of Nogo and NgR in retina and optical nerve of glaucomatous would evoke and bring a new way of the rehabilitative treatmentObjectiveTo observe the mean of the intraocular pressure (IOP)of normal rats, and the fluctuation in the daytime, and develop a distinctive model of the chronic glaucoma with optic neuropath induced by intraocular hypertension in rats.To investigated the distribution...