Date Thesis Awarded


Access Type

Honors Thesis -- Access Restricted On-Campus Only

Degree Name

Bachelors of Science (BS)




Margaret S. Saha

Committee Members

Gregory D. Smith

Eric L. Bradley

Randolph A. Coleman

Joshua A. Burk


While the role of transcriptional and signaling cascades has been well-characterized in neuronal fate acquisition, little is known about the role of spontaneous calcium transients in early neural development or the channels that mediate this activity. We hypothesized that calcium activity plays a key role in regulating neuronal phenotype specification and that L-type voltage-gated calcium channels mediate this activity. Towards this end, we investigated the role of calcium activity in neurotransmitter phenotype acquisition on the single cell level during different developmental stages to correlate a single cell’s spontaneous calcium activity with its neurotransmitter phenotype. We also investigated the proposed mediating effect of L-type VGCCs with a pharmacological approach. When compared with cells negative for VGlut, NBT, or GAD, cells that expressed these genes spiked significantly less across the examined stages. This correlation was also found when comparing spiking activity of cells positive or negative for VGCC α subunits. Interestingly, cells positive for VGlut exhibited higher levels of spiking activity than those positive for GAD. In terms of pharmacological manipulation, a lower micromolar amount of antagonist, diltiazem, decreased the number of calcium transients, whereas exposure to a higher concentration led to an overall increase in calcium activity. Exposure to an agonist, Bay K8644, did not significantly increase calcium activity. We also investigated the possibility that preventing cell-cell interactions following tissue dissociation may keep cells in neuronal progenitor states and found that the majority of cells negative for VGlut, NBT, GAD, or the VGCC alpha subunits were indeed in a progenitor state.

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Creative Commons License
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