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Voltage dependence and activation mechanisms of the neuromodulatory inward current (IMI) in the stomatogastric ganglion of C. borealis
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Gray, Michael. Voltage dependence and activation mechanisms of the neuromodulatory inward current (IMI) in the stomatogastric ganglion of C. borealis. Retrieved from https://doi.org/doi:10.7282/T3GT5Q5J

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TitleVoltage dependence and activation mechanisms of the neuromodulatory inward current (IMI) in the stomatogastric ganglion of C. borealis
NameGray, Michael (author); Nadim, Farzan (chair); Tepper, James (internal member); Kim, Haesun (internal member); Baro, Deborah (outside member); Rutgers University; Graduate School - Newark
Date Created2015
Other Date2015-10 (degree)
SubjectNeuroscience
Extent1 online resource (xi, 312 p. : ill.)
DescriptionThe Neuromodulatory Inward Current (IMI) of the stomatogastric ganglion (STG) in Cancer borealis is an inward difference current elicited by neuromodulators whose current voltage relation (IV curve) has been shown to be crucial to transitioning the pyloric network of this system from non-oscillating to oscillating states. Here, models of the second messenger signaling of both this current’s activation and voltage dependence are constructed and tested. First, we examine how the proctolin receptor activates IMI with the hypothesis that it signals through an intermediate signaling component. This is tested by bath application and pressure injection of agonists and antagonists of second messenger systems and examining their effect on neuromodulator induced IMI. Consistent with this hypothesis, it is found that this proctolin-induced IMI is sensitive to modulators of G-protein function. Also consistent with this hypothesis, it is found that proctolin-induced IMI is sensitive to modulators of intracellular calcium concentration and calmodulin activated kinases. In contrast, there seems to be no effect to acute applications of pharmaceutical activators and inhibitors of cyclic nucleotides, Phospholipase C, and receptor tyrosine kinase signaling. Next, we examine the mechanism of IMI voltage dependence that has been shown to be dependent upon extracellular calcium level and calmodulin signaling which we show is necessary for IMI voltage dependence by finding that application of calmodulin antagonists in normal calcium reduces IMI voltage dependence. However, it is found that calmodulin activators do not rescue IMI voltage dependence in low calcium so we propose that a Calcium Sensitive Receptor (CaSR) maintains IMI voltage dependence by active detection of extracellular calcium. This hypothesis is supported by several lines of evidence. First, IMI slope was increased by the specific calcium sensitive receptor antagonist NPS-2143 suggesting CaSR involvement. Second, IMI slope conductance was increased by exposure to the βγ-subunit inhibitor, gallein, suggesting that voltage dependence can be modulated by the βγ-subunit of trimeric g-proteins. Third, W7 induced linearization of IMI was reduced by pre-incubation of preparations with endocytosis inhibitors, suggesting that downregulation of a receptor is mediating W7 induced changes in IMI voltage dependence. Together, these results support the hypothesis that IMI voltage dependence is mediated at least in part by a CaSR-like G-protein coupled receptor (GPCR).
NotePh.D.
NoteIncludes bibliographical references
Noteby Michael Gray
Genretheses, ETD doctoral
Persistent URLhttps://doi.org/doi:10.7282/T3GT5Q5J
Languageeng
CollectionGraduate School - Newark Electronic Theses and Dissertations
Organization NameRutgers, The State University of New Jersey
RightsThe author owns the copyright to this work.
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