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dc.contributor.advisorFregosi, Ralphen
dc.contributor.authorYoung, Cristina Teresa
dc.creatorYoung, Cristina Teresaen
dc.date.accessioned2017-08-11T17:56:56Z
dc.date.available2017-08-11T17:56:56Z
dc.date.issued2017
dc.identifier.citationYoung, Cristina Teresa. (2017). Prenatal Nicotine Exposure and the 5HTα -7 Receptor (Bachelor's thesis, University of Arizona, Tucson, USA).
dc.identifier.urihttp://hdl.handle.net/10150/625257
dc.description.abstractPrenatal nicotine exposure is a know risk factor for Sudden Infant Death Syndrome (SIDS). This risk increase is thought to be the result of developmental nicotine exposure (DNE) affecting the development of the brains control of breathing. This experiment was executed to determine what affect, if any, this type of nicotine exposure would have on the serotonin (5HT) system, specifically the 5HT alpha-7 receptor. Prenatal rat pups were exposed to nicotine using osmotic mini-pumps during pregnancy, with continued exposure through breast milk after birth (DNE). Brainstem-spinal cord preparations from 1-5 day old pups, both DNE and an unexposed control group, were placed into a split-bath and drugs where administered to either the brainstem or the spinal cord. The frequency and amplitude of action potential burst were measured in the brainstem (rostral) experiments and tonic activity was measured in the spinal cord (caudal) experiments. Both experiments followed the same drug application protocol. A baseline of ten minutes was established, followed by fifteen minutes of 5HTα-7 antagonist application, followed by thirty minutes of 5HTα-7 antagonist + 5HT application, followed by washout for twenty minutes. DNE exposure had statistically significant affects in the rostral experiments, but produced non-significant trends in the caudal experiments.
dc.language.isoen_USen
dc.publisherThe University of Arizona.en
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
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.titlePrenatal Nicotine Exposure and the 5HTα -7 Receptoren_US
dc.typetexten
dc.typeElectronic Thesisen
thesis.degree.grantorUniversity of Arizonaen
thesis.degree.levelbachelorsen
thesis.degree.disciplineHonors Collegeen
thesis.degree.disciplinePhysiologyen
thesis.degree.nameB.S.en
refterms.dateFOA2018-09-11T22:19:51Z
html.description.abstractPrenatal nicotine exposure is a know risk factor for Sudden Infant Death Syndrome (SIDS). This risk increase is thought to be the result of developmental nicotine exposure (DNE) affecting the development of the brains control of breathing. This experiment was executed to determine what affect, if any, this type of nicotine exposure would have on the serotonin (5HT) system, specifically the 5HT alpha-7 receptor. Prenatal rat pups were exposed to nicotine using osmotic mini-pumps during pregnancy, with continued exposure through breast milk after birth (DNE). Brainstem-spinal cord preparations from 1-5 day old pups, both DNE and an unexposed control group, were placed into a split-bath and drugs where administered to either the brainstem or the spinal cord. The frequency and amplitude of action potential burst were measured in the brainstem (rostral) experiments and tonic activity was measured in the spinal cord (caudal) experiments. Both experiments followed the same drug application protocol. A baseline of ten minutes was established, followed by fifteen minutes of 5HTα-7 antagonist application, followed by thirty minutes of 5HTα-7 antagonist + 5HT application, followed by washout for twenty minutes. DNE exposure had statistically significant affects in the rostral experiments, but produced non-significant trends in the caudal experiments.


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