Resource allocation and hormone provisioning during vitellogenesis has been documented for many oviparous reptiles, while viviparous species remain relatively understudied in the context of yolk composition. Squamates that have evolved viviparity have retained varying degrees of embryonic nourishment via the yolk (lecithotrophy). Very little is known about the timing of embryonic hormone production, and the degree of maternal hormone provisioning in viviparous reptiles. Viviparous species may, in principle, receive hormone exposure through some or all of three routes, viz., maternal provisioning in the yolk, transfer from the maternal circulation, and/or hormone production by the developing embryonic endocrine tissues. In toad-eating snakes, adrenal hormones may provide protection from toad toxins, supplementing genetic resistance. Additionally, one species of oviparous snake has been shown to provision its embryos with defensive toxins from toads. We hypothesized that embryonic hormone levels would increase during development and that yolk hormone levels would correspondingly decrease. We also predicted that the embryos from females administered toad toxin would have higher levels of corticosterone (CORT) in response to exposure to a toad toxin. We measured levels of CORT in the embryos and corresponding yolks of a viviparous and genetically toxin-resistant natricine, the Western Terrestrial Garter Snake (Thamnophis elegans), beginning at Zehr Stage 26. We found that embryos and their corresponding yolks had relatively higher levels of CORT in later stages. There were no measurable differences in CORT between embryos of the same stage obtained from dams treated with marinobufagenin (MBG) or no treatment. Given that yolk and embryonic CORT increase throughout the course of development, a trade-off between early maternal provisioning and the onset of adrenal function is not apparent. However, increase in adrenal production of CORT over the course of development remains relevant to both stress physiology and physiological toxin resistance.