Date of Award:

8-2023

Document Type:

Dissertation

Degree Name:

Doctor of Philosophy (PhD)

Department:

Biology

Committee Chair(s)

Alan H. Savitzky

Committee

Alan H. Savitzky

Committee

Susannah French

Committee

Karen Kapheim

Committee

Molly Womack

Committee

Shabnam Mohammadi

Abstract

The long observed relationship between enlarged adrenal glands and toad-eating in snakes has remained a mystery in physiological ecology and herpetology. It has been predicted that large adrenal glands may be capable of producing higher amounts of key hormones, and that higher plasma hormone levels may lend some behavioral or physiological benefits after a toxic toad has been eaten. I address questions surrounding adrenal enlargement and its potential benefits to toad eaters in four research chapters. In my second chapter, I quantify adrenal hormone output at different embryonic stages in the toad-generalist snake Thamnophis elegans and examine the ability of mid stage embryos to respond hormonally when their mothers are given a high dose of toad toxin. I found that adrenal hormones increase in both the embryo and the yolk as they develop, and that toad toxin given to mothers did not have a significant impact on embryo or yolk hormone levels. In my third chapter I compared the ratio of different cell types in the adrenal gland between a toad specialist species, toad-generalist species, and non-toad eating species. I found that the toad specialists had a higher ratio of interrenal cells (cells that produce corticosteroids). This could indicate that toad specialists are able to produce higher levels of corticosteroids when poisoned. I also examined sex differences within each species and found that the cell-type ratios within the non toad-eating species was significant. This surprising finding could be due to behavioral and life history differences between males and females of the non toad-eating species. In my fourth chapter I measured the corticosterone response of the toad specialist Heterodon platirhinos upon capture (before plasma hormone levels can rise) and after a field stress test. The hormone corticosterone aids in energy mobilization and increases significantly in response to stressful events. I found that corticosterone does increase significantly in this species in response to a stress test. Comparisons with stress tests in other snake species also show that the species H. platirhinos can respond to a stressful event with relatively higher levels of corticosterone. This could indicate that a larger adrenal gland is capable of releasing more hormones into the bloodstream, this may carry implications for physiological toxin resistance in toad-eating snakes. My final research chapter examined the relationship between the adrenal hormone aldosterone and the expression of a toad toxin resistant ion exchanger, ATP1a3. In other animals, the adrenal hormone aldosterone has been shown to increase the gene expression of ATP1a3. I gave snakes a high dose of the hormone aldosterone and measured gene expression. The hormone treatment did not significantly increase the expression of this gene, but other pathways should not be ruled out. It is possible that adrenal hormones may provide some benefit at the molecular level through other mechanisms. Additionally, I measured brain ATP1a3 expression and found that it was comparable to heart expression, which was previously found to be high relative to other organ tissues. Overall, these experiments show that adrenal enlargement does appear to impact the secretion capability of the gland in species with adrenal enlargement and emphasize the many potential ways that this could impact an animal’s physiology across multiple tiers of organismal biology.

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