Mechanisms of Depolarization Induced Dendritic Growth of Drosophila Motor Neurons

Persistent Link:
http://hdl.handle.net/10150/195475
Title:
Mechanisms of Depolarization Induced Dendritic Growth of Drosophila Motor Neurons
Author:
Cherry, Cortnie Lauren
Issue Date:
2006
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
MECHANISMS OF DEPOLARIZATION INDUCED DENDRITIC GROWTH OF DROSOPHILA MOTOR NEURONS Cortnie Lauren Cherry The University of Arizona, 2006 Director: Richard B. Levine The study of the cellular mechanisms underlying dendritic growth contributes to our understanding of nervous system development, function and disease. Electrical activity is a fundamental property of neurons, and this property is utilized to influence the mechanisms involved in dendrite formation and maturation. Here we employ the Drosophila transgenic system to quantify dendritic growth of identified motor neurons using both in vitro and in vivo techniques. Two novel techniques are introduced: one a system to visualize and measure dendritic outgrowth in cultured neurons using reporter proteins, and the other using 3D reconstruction to measure the arborization of identified motor neurons in vivo. Both transgenic manipulation of K+ channel function and depolarizing concentrations of K+ in the culture medium result in an acceleration of dendritic outgrowth. Depolarization induced outgrowth is dependent on Plectreurys Toxin (PLTX)-sensitive voltage-gated calcium current and protein synthesis in cultured motor neurons. Depolarization leads to direct induction of fos, a protein that heterodimerizes with jun to make the functional transcription factor, AP-1. Fos, but not jun, is necessary for basal levels of dendritic growth, while both are necessary for depolarization induced outgrowth. Over-expression of AP-1 in control cells is sufficient to cause dendritic outgrowth. The transcription factor Adf-1 is also necessary for basal and depolarization induced growth, but unlike AP-1 is not sufficient to cause outgrowth when over-expressed. Another transcription factor CREB, on the other hand, is not necessary for basal levels of dendritic growth, but is necessary for depolarization induced dendritic growth. Over-expression of CREB, like Adf-1, is not sufficient to cause dendritic outgrowth. These findings present exciting new techniques for the study of the field of dendritic regulation and contribute to our understanding of the cellular mechanisms underlying dendritic growth.
Type:
text; Electronic Dissertation
Keywords:
Drosphila; neuron; activity; calcium; AP-1; depolarization
Degree Name:
PhD
Degree Level:
doctoral
Degree Program:
Physiological Sciences; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Levine, Richard B.
Committee Chair:
Levine, Richard B.

Full metadata record

DC FieldValue Language
dc.language.isoENen_US
dc.titleMechanisms of Depolarization Induced Dendritic Growth of Drosophila Motor Neuronsen_US
dc.creatorCherry, Cortnie Laurenen_US
dc.contributor.authorCherry, Cortnie Laurenen_US
dc.date.issued2006en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractMECHANISMS OF DEPOLARIZATION INDUCED DENDRITIC GROWTH OF DROSOPHILA MOTOR NEURONS Cortnie Lauren Cherry The University of Arizona, 2006 Director: Richard B. Levine The study of the cellular mechanisms underlying dendritic growth contributes to our understanding of nervous system development, function and disease. Electrical activity is a fundamental property of neurons, and this property is utilized to influence the mechanisms involved in dendrite formation and maturation. Here we employ the Drosophila transgenic system to quantify dendritic growth of identified motor neurons using both in vitro and in vivo techniques. Two novel techniques are introduced: one a system to visualize and measure dendritic outgrowth in cultured neurons using reporter proteins, and the other using 3D reconstruction to measure the arborization of identified motor neurons in vivo. Both transgenic manipulation of K+ channel function and depolarizing concentrations of K+ in the culture medium result in an acceleration of dendritic outgrowth. Depolarization induced outgrowth is dependent on Plectreurys Toxin (PLTX)-sensitive voltage-gated calcium current and protein synthesis in cultured motor neurons. Depolarization leads to direct induction of fos, a protein that heterodimerizes with jun to make the functional transcription factor, AP-1. Fos, but not jun, is necessary for basal levels of dendritic growth, while both are necessary for depolarization induced outgrowth. Over-expression of AP-1 in control cells is sufficient to cause dendritic outgrowth. The transcription factor Adf-1 is also necessary for basal and depolarization induced growth, but unlike AP-1 is not sufficient to cause outgrowth when over-expressed. Another transcription factor CREB, on the other hand, is not necessary for basal levels of dendritic growth, but is necessary for depolarization induced dendritic growth. Over-expression of CREB, like Adf-1, is not sufficient to cause dendritic outgrowth. These findings present exciting new techniques for the study of the field of dendritic regulation and contribute to our understanding of the cellular mechanisms underlying dendritic growth.en_US
dc.typetexten_US
dc.typeElectronic Dissertationen_US
dc.subjectDrosphilaen_US
dc.subjectneuronen_US
dc.subjectactivityen_US
dc.subjectcalciumen_US
dc.subjectAP-1en_US
dc.subjectdepolarizationen_US
thesis.degree.namePhDen_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplinePhysiological Sciencesen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorLevine, Richard B.en_US
dc.contributor.chairLevine, Richard B.en_US
dc.contributor.committeememberKarunanithi, Shankeren_US
dc.contributor.committeememberRance, Naomien_US
dc.contributor.committeememberWilson, Jeanen_US
dc.contributor.committeememberYool, Andreaen_US
dc.identifier.proquest1738en_US
dc.identifier.oclc659747491en_US
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