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Premature birth is a global problem, affecting both developed and undeveloped countries including the United States. A crucial aspect of both preterm and term birth is remodeling of the cervix. Despite the large scale of the problem, factors leading to the initiation of remodeling are largely unknown. The present study examined the role of the cholinergic anti-inflammatory pathway, with particular focus on the nicotinic receptor, and its role in driving remodeling and preterm birth. Mice were treated with either vehicle control, mecamylamine (a nonspecific nicotinic receptor antagonist), RU486 (a progesterone receptor antagonist) as a preterm control, or progesterone (a hormone involved in the timing of birth) as a delayed birth control, using an novel thermogel treatment delivery method (TIM). Animals were sacrificed post partum and their cervixes were stained to analyze cell nuclei density and macrophage content, two factors expected to change during remodeling and parturition. Though the TIM was effective in delivering the drug treatments, mecamylamine did not cause preterm birth or a change in macrophage content and cell nuclei density. The results of this experiment indicate that the nicotinic receptor does not play a role in driving remodeling or preterm birth. Though the treatment did not yield significant results, the effectiveness of the TIM means that it may be developed into the first minimally invasive direct to cervix treatment in humans.