Glaucoma Modeling & Pharmacodynamics Services

• NMDA-Induced Retinal Ganglion Cells (RGCs) Injury Models

N-methyl-D-aspartic acid (NMDA), an amino acid derivative acting as an excitatory neurotransmitter, plays a crucial role in neuronal signaling. Activation of NMDA receptors induces an influx of calcium ions within retinal ganglion cells (RGCs), precipitating cellular demise. Following the intravitreal administration of NMDA in murine models, observable signs of cell pyknosis emerge within just one hour. Subsequently, the associated Thy-1 mRNA levels in the retina commence a decline at the six-hour mark, culminating in the death of retinal ganglion cells approximately 24 hours post-injection.

• Optic Nerve Clamp Induced Optic Nerve Injury Models

Following the induction of anesthesia in the rat, the procedure progresses under a binocular surgical microscope: an incision is created at the lateral canthus. Subsequently, the Tenon's capsule is incised to expose the underlying structures. The lateral rectus muscle is then carefully isolated and transected. Employing blunt dissection techniques, the surgical field extends along the temporal scleral surface toward the optic nerve. A small vascular clamp is then strategically positioned on the optic nerve posterior to the globe for a specified period, thereby establishing a model of optic nerve crush injury in the rat.

• Hypertonic Saline Injection Models

Administering hypertonic saline into the episcleral veins induces sclerosis of the trabecular meshwork, thereby enhancing resistance to aqueous humor outflow and subsequently elevating intraocular pressure in experimental animal models. Utilizing a glass micropipette linked to a syringe, hypertonic saline is meticulously injected into the scleral vein of rats. Within a timeframe of 7 to 10 days post-injection, necrosis of the trabecular meshwork ensues, obstructing the aqueous humor's egress and resulting in heightened intraocular pressure. This elevation can be sustained for as long as 200 days.

• Spontaneous Glaucoma Mouse Models

The DBA/2J mouse model epitomizes the study of spontaneous glaucoma. In DBA/2J mice, apoptosis of retinal ganglion cells alongside optic nerve degeneration commences between 8 and 9 months of age. By the time these mice reach 18 months, over 90% of the optic nerve exhibits severe degeneration, with visual capabilities nearly entirely diminished. The apoptosis rate in retinal ganglion cells can exceed 90%, positioning DBA/2J mice as an exceptional experimental model for investigating glaucoma pathophysiology and potential therapeutic interventions.

• Anterior Chamber Injection Model

Injecting specific substances into the anterior chamber of experimental animals, such as sodium hyaluronate, methylcellulose, etc., increases the outflow resistance of aqueous humor or blocking the trabecular meshwork, thereby slowing or blocking the outflow of aqueous humor, resulting in increased intraocular pressure. A single injection of hyaluronic acid into the anterior chamber of rats for 5 days can form an acute high intraocular pressure model. If the injection is repeated once a week for 9 weeks, a chronic high intraocular pressure model can be formed.