Cultured trabecular meshwork (TM) cells are a valuable model system to study the cellular mechanisms involved in the regulation of conventional outflow resistance and thus intraocular pressure; and their dysfunction resulting in ocular hypertension. In this review, we describe the standard procedures used for the isolation of TM cells from several animal species including humans, and the methods used to validate their identity. Having a set of standard practices for TM cells will increase the scientific rigor when used as a model, and enable other researchers to replicate and build upon previous findings.

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J. Neurochem. (2011) 118, 224–236. Abstract Physical exercise produces a variety of psychophysical effects, including altered pain perception. Elevated levels of centrally produced endorphins or endocannabinoids are implicated as mediators of exercise‐induced analgesia. The effect of exercise on the development and persistence of disease‐associated acute/chronic pain remains unclear. In this study, we quantified the physiological consequence of forced‐exercise on the development of diabetes‐associated neuropathic pain. Euglycemic control or streptozotocin (STZ)‐induced diabetic adult male rats were subdivided into sedentary or forced‐exercised (2–10 weeks, treadmill) subgroups and assessed for changes in tactile responsiveness. Two weeks following STZ‐treatment, sedentary rats developed a marked and sustained hypersensitivity to von Frey tactile stimulation. By comparison, STZ‐treated diabetic rats undergoing forced‐exercise exhibited a 4‐week delay in the onset of tactile hypersensitivity that was independent of glucose control. Exercise‐facilitated analgesia in diabetic rats was reversed, in a dose‐dependent manner, by naloxone. Small‐diameter (< 30 μm) DRG neurons harvested from STZ‐treated tactile hypersensitive diabetic rats exhibited an enhanced (2.5‐fold) rightward (depolarizing) shift in peak high‐voltage activated (HVA) Ca2+ current density with a concomitant appearance of a low‐voltage activated (LVA) Ca2+ current component. LVA Ca2+ currents present in DRG neurons from hypersensitive diabetic rats exhibited a marked depolarizing shift in steady‐state inactivation. Forced‐exercise attenuated diabetes‐associated changes in HVA Ca2+ current density while preventing the depolarizing shift in steady‐state inactivation of LVA Ca2+ currents. Forced‐exercise markedly delays the onset of diabetes‐associated neuropathic pain, in part, by attenuating associated changes in HVA and LVA Ca2+ channel function within small‐diameter DRG neurons possibly by altering opioidergic tone.