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Voltage dependence and activation mechanisms of the neuromodulatory inward current (IMI) in the stomatogastric ganglion of C. borealis
Descriptive
TitleInfo
Title
Voltage dependence and activation mechanisms of the neuromodulatory inward current (IMI) in the stomatogastric ganglion of C. borealis
Name
(type = personal)
NamePart
(type = family)
Gray
NamePart
(type = given)
Michael
NamePart
(type = date)
1979-
DisplayForm
Michael Gray
Role
RoleTerm
(authority = RULIB)
author
Name
(type = personal)
NamePart
(type = family)
Nadim
NamePart
(type = given)
Farzan
DisplayForm
Farzan Nadim
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
chair
Name
(type = personal)
NamePart
(type = family)
Tepper
NamePart
(type = given)
James
DisplayForm
James Tepper
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Kim
NamePart
(type = given)
Haesun
DisplayForm
Haesun Kim
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Baro
NamePart
(type = given)
Deborah
DisplayForm
Deborah Baro
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
outside member
Name
(type = corporate)
NamePart
Rutgers University
Role
RoleTerm
(authority = RULIB)
degree grantor
Name
(type = corporate)
NamePart
Graduate School - Newark
Role
RoleTerm
(authority = RULIB)
school
TypeOfResource
Text
Genre
(authority = marcgt)
theses
Genre
(authority = ExL-Esploro)
ETD doctoral
OriginInfo
DateCreated
(encoding = w3cdtf);
(qualifier = exact)
2015
DateOther
(qualifier = exact);
(type = degree)
2015-10
CopyrightDate
(encoding = w3cdtf);
(qualifier = exact)
2015
Place
PlaceTerm
(type = code)
xx
Language
LanguageTerm
(authority = ISO639-2b);
(type = code)
eng
Abstract
(type = abstract)
The 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).
Subject
(authority = RUETD)
Topic
Neuroscience
RelatedItem
(type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
RelatedItem
(type = host)
TitleInfo
Title
Graduate School - Newark Electronic Theses and Dissertations
Identifier
(type = local)
rucore10002600001
Identifier
ETD_6647
Identifier
(type = doi)
doi:10.7282/T3GT5Q5J
PhysicalDescription
Form
(authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (xi, 312 p. : ill.)
Note
(type = degree)
Ph.D.
Note
(type = bibliography)
Includes bibliographical references
Note
(type = statement of responsibility)
by Michael Gray
Location
PhysicalLocation
(authority = marcorg);
(displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
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Rights
RightsDeclaration
(ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder
(type = personal)
Name
FamilyName
Gray
GivenName
Michael
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime
(encoding = w3cdtf);
(qualifier = exact);
(point = start)
2015-08-06 12:06:00
AssociatedEntity
Name
Michael Gray
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - Newark
AssociatedObject
Type
License
Name
Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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Technical
RULTechMD
(ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem
(VERSION = 5.1)
windows xp
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