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The potential role of an abnormally low (orbital) cerebrospinal fluid pressure (CSFP) as one of the two determinants of the trans-lamina cribrosa paressure difference has increasingly been discussed in recent studies and articles. A major obstacle to further research on the CSFP as a potential part of the pathogenesis of glaucomatous optic neuropathy has so far been the lack of appropriate and generally available animal models. Chowdhury, Holman and Fautsch developed a novel rat model, in which 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 then modulated manually by adjusting the height of a column filled with artificial cerebrospinal fluid in relation to the animal's head. Brown Norway rats (n = 5) maintained the cannula in the lateral ventricles for approximately four weeks while in two of three Sprague-Dawley animals, the cap was dislodged within one week. Surgical placement of the cannula into the cisterna magna of Brown Norway rats (n = 6) resulted in decreased survival and increased neurological compromise. Based on the ability to maintain an implanted cannula for at least four weeks with minimal surgical issues, the Brown Norway rat with a stainless steel cannula inserted into the lateral ventricle became the animal of choice for all subsequent experiments.