Experimental glaucoma model with controllable intraocular pressure history
Autor: | Kayla R. Ficarrotta, Christopher L. Passaglia, Youssef Mohamed |
---|---|
Rok vydání: | 2020 |
Předmět: |
Male
Retinal Ganglion Cells 0301 basic medicine Aqueous outflow medicine.medical_specialty Intraocular pressure genetic structures lcsh:Medicine Ocular hypertension Glaucoma Retinal ganglion Article 03 medical and health sciences 0302 clinical medicine Ophthalmology Animals Medicine lcsh:Science Intraocular Pressure Multidisciplinary business.industry lcsh:R Optic Nerve medicine.disease Cannula eye diseases Rats Experimental models of disease Disease Models Animal 030104 developmental biology Time course 030221 ophthalmology & optometry lcsh:Q Outflow sense organs business |
Zdroj: | Scientific Reports Scientific Reports, Vol 10, Iss 1, Pp 1-12 (2020) |
ISSN: | 2045-2322 |
Popis: | Glaucoma-like neuropathies can be experimentally induced by disturbing aqueous outflow from the eye, resulting in intraocular pressure (IOP) changes that are variable in magnitude and time course and permanent in duration. This study introduces a novel method of glaucoma induction that offers researchers round-the-clock measurement and reversible control of IOP for the first time. One eye of Brown-Norway rats was implanted with a cannula tethered to a pressure sensor and aqueous reservoir. IOP was raised 10 mmHg for weeks-to-months in treated animals and unaltered in control animals. Counts of Brn3a-expressing retinal ganglion cells (RGCs) in implanted eyes were indistinguishable from non-implanted eyes in control animals and 15 ± 2%, 23 ± 4%, and 38 ± 4% lower in animals exposed to 2, 4, and 9 weeks of IOP elevation. RGC loss was greater in peripheral retina at 2 weeks and widespread at longer durations. Optic nerves also showed progressive degeneration with exposure duration, yet conventional outflow facility of implanted eyes was normal (24.1 ± 2.9 nl/min/mmHg) even after 9-weeks elevation. Hence, this infusion-based glaucoma model exhibits graded neural damage with unimpaired outflow pathways. The model further revealed a potentially-significant finding that outflow properties of rat eyes do not remodel in response to chronic ocular hypertension. |
Databáze: | OpenAIRE |
Externí odkaz: |