Persistent Link:
http://hdl.handle.net/10150/243692
Title:
Neurochemical Changes Following Activation of the Dural Afferent
Author:
Ahmed, Sarah Rubis
Issue Date:
May-2012
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:
The objective of the study was to explore the neurochemical effects of dural afferent activation in different regions of the brain, the ventral tegmental area (VTA) and the nucleus accumbens (NAcc), and determine how these mechanisms play a role in pain relief following onset of migraine pain. Inflammatory mediators (IM) or synthetic interstitial fluid (SIF) were injected into the dura of rats to initiate dural afferent activation, followed by treatments of saline (Sal) or lidocaine (Lido) injection into the rostral ventromedial medulla (RVM). Upon collection of VTA and NAcc tissue sections from each treatment group, cells were immunolabeled for FOS to determine action potential prevalence associated with dopamine release. VTA showed increased FOS expression in rats treated with IM + Sal, while NAcc showed greater expression in IM + Lido treatment group. These effects may be characteristic of the role of lidocaine within the reward system, although signaling within the dopaminergic system may be altered upon projection into the NAcc region. These findings are consistent with the possibility of outside factors of signal propagation throughout the dopaminergic system. Further research on the underlying mechanisms of the dopaminergic system may provide novel treatment strategies of migraine pain relief.
Type:
text; Electronic Thesis
Degree Name:
B.S.
Degree Level:
bachelors
Degree Program:
Honors College; Physiology
Degree Grantor:
University of Arizona

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleNeurochemical Changes Following Activation of the Dural Afferenten_US
dc.creatorAhmed, Sarah Rubisen_US
dc.contributor.authorAhmed, Sarah Rubisen_US
dc.date.issued2012-05-
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.abstractThe objective of the study was to explore the neurochemical effects of dural afferent activation in different regions of the brain, the ventral tegmental area (VTA) and the nucleus accumbens (NAcc), and determine how these mechanisms play a role in pain relief following onset of migraine pain. Inflammatory mediators (IM) or synthetic interstitial fluid (SIF) were injected into the dura of rats to initiate dural afferent activation, followed by treatments of saline (Sal) or lidocaine (Lido) injection into the rostral ventromedial medulla (RVM). Upon collection of VTA and NAcc tissue sections from each treatment group, cells were immunolabeled for FOS to determine action potential prevalence associated with dopamine release. VTA showed increased FOS expression in rats treated with IM + Sal, while NAcc showed greater expression in IM + Lido treatment group. These effects may be characteristic of the role of lidocaine within the reward system, although signaling within the dopaminergic system may be altered upon projection into the NAcc region. These findings are consistent with the possibility of outside factors of signal propagation throughout the dopaminergic system. Further research on the underlying mechanisms of the dopaminergic system may provide novel treatment strategies of migraine pain relief.en_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.nameB.S.en_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
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