The nucleus pulposus (NP) plays a critical role in resisting loads placed on the spine, and therefore, the intervertebral disc. The function of the NP is to generate a hydrostatic pressure to evenly disperse the load within the disc. This ability hinges on the hydration of the disc, which is affected by age, health and even prior load history. This dissertation aims to elucidate key points about how the disc functions and reacts, both mechanically and biologically, to different sets of axial loading. We demonstrate our ability to create a degenerate disc model using trans-annular puncture in caudal rat discs and verify using viscoelastic analysis and histologic examination. Using a custom miniature fiber-optic pressure sensor, we determined the loss of pressurization in a degenerate versus a healthy disc. This compromised ability to generate an intradiscal pressure is essential, and indicates that a degenerate disc inadequately distributes the load and may lead to pain, injury and lack of function. We then investigated the influence of load history on the NP. Using a preload placed on a disc beforehand, we change the hydrated state of the disc before the exertion load is applied. The viscoelastic creep response was analyzed and showed changes due to the addition of the preload. We also directly observed this change by using the miniature pressure sensors to measure intradiscal pressure during the loading regime. To further track changes caused by the introduction of a preload, we examined the gene expression of several associated extracellular matrix proteins after loading. The results demonstrate changing gene expression contrary to the expected outcome, given the understood pressurized cellular environment. We speculate that instead of a hydrostatic pressure driven response, the tonic environment dictated genetic upregulation. Using collaborative efforts, we assessed the ability to use Pneumatic Artificial Muscles as the actuating element in a long term loading device for caudal rat discs. In conclusion, we gathered new reactions from the NP given a variety of changed states, both diseased and loaded. Our new findings will help complete the picture to fully understand how the disc functions, specifically the response of the NP