Abstract
Reduced intracranial pressure is considered a risk factor for glaucomatous optic neuropathies. All current data supporting intracranial pressure as a glaucoma risk factor comes from retrospective and prospective studies. Unfortunately, there are no relevant animal models for investigating this link experimentally. Here we report a novel rat model that can be used to study the role of intracranial pressure modulation on optic neuropathies. Stainless steel cannulae were inserted into the cisterna magna or the lateral ventricle of Sprague-Dawley and Brown Norway rats. The cannula was attached to a pressure transducer connected to a computer that recorded intracranial pressure in real-time. Intracranial pressure was modulated manually by adjusting the height of a column filled with artificial cerebrospinal fluid in relation to the animal’s head. After data collection the morphological appearance of the brain tissue was analyzed. Based on ease of surgery and ability to retain the cannula, Brown Norway rats with the cannula implanted in the lateral ventricle were selected for further studies. Baseline intracranial pressure for rats was 5.5±1.5 cm water (n=5). Lowering of the artificial cerebrospinal fluid column by 2 cm and 4 cm below head level reduced ICP to 3.7±1.0 cm water (n=5) and 1.5±0.6 cm water (n=4), a reduction of 33.0% and 72.7% below baseline. Raising the cerebrospinal fluid column by 4 cm increased ICP to 7.5±1.4 cm water (n=2) corresponding to a 38.3% increase in intracranial pressure. Histological studies confirmed correct cannula placement and indicated minimal invasive damage to brain tissues. Our data suggests that the intraventricular cannula model is a unique and viable model that can be used to study the effect of altered intracranial pressure on glaucomatous optic neuropathies.
Highlights
Glaucoma, the leading cause of irreversible blindness, is a progressive neurodegenerative disease with a complex and incompletely understood pathophysiology[1,2,3]
Elevated intraocular pressure (IOP) is not observed in normal tension glaucoma (NTG) damage to the optic nerve still occurs[6]
Selection of appropriate rat strain for use in the intraventricular cannula model Both Sprague Dawley and Brown Norway rats were able to maintain the cannula in the lateral ventricles
Summary
The leading cause of irreversible blindness, is a progressive neurodegenerative disease with a complex and incompletely understood pathophysiology[1,2,3]. An increased intraocular pressure (IOP) is the most prevalent risk factor for glaucoma and is generally believed to be a primary causal factor for neuronal cell damage in the optic nerve head[1,5,6,7]. Exceptions to this correlation between elevated IOP and glaucomatous optic nerve damage have been noted. Elevated IOP is not observed in normal tension glaucoma (NTG) damage to the optic nerve still occurs[6]. Individuals with elevated IOP do not always develop glaucoma and optic nerve damage[8]
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