Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/41422
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dc.contributor.authorZeitzer, J.M.
dc.contributor.authorMorales-Villagran, A.
dc.contributor.authorMaidment, N.T.
dc.contributor.authorBehnke, E.J.
dc.contributor.authorAckerson, L.C.
dc.contributor.authorLopez-Rodriguez, F.
dc.contributor.authorFried, I.
dc.contributor.authorEngel Jr., J.
dc.contributor.authorWilson, C.L.
dc.date.accessioned2015-09-15T17:57:02Z-
dc.date.available2015-09-15T17:57:02Z-
dc.date.issued2006
dc.identifier.urihttp://www.scopus.com/inward/record.url?eid=2-s2.0-33745793420&partnerID=40&md5=04734706fe1c12573c636dbcc0619abb
dc.identifier.urihttp://hdl.handle.net/20.500.12104/41422-
dc.description.abstractStudy Objectives: To examine the pattern of extracellular adenosine in the human brain during sleep deprivation, sleep, and normal wake. Design: Following recovery from implantation of clinical depth electrodes, epilepsy patients remained awake for 40 continuous hours, followed by a recovery sleep episode. Setting: Neurology ward at UCLA Medical Center. Patients or Participants: Seven male epilepsy patients undergoing depth electrode localization of pharmacologically refractory seizures. Interventions: All subjects were implanted with depth electrodes, a subset of which were customized to contain microdialysis probes. Microdialysis samples were collected during normal sleep, sleep deprivation, and recovery sleep from human amygdalae (n=8), hippocampus (n=1), and cortex (n=1). Measurements and Results: In none of the probes did we observe an increase in extracellular adenosine during the sleep deprivation. There was a significant, though very small, diurnal oscillation (2.5%) in 5 of the 8 amygdalae. There was no effect of epileptogenicity on the pattern of extracellular adenosine. Conclusions: Our observations, along with those in animal studies, indicate that the role of extracellular adenosine in regulating sleep pressure is not a global brain phenomenon but is likely limited to specific basal forebrain areas. Thus, if energy homeostasis is a function of sleep, an increased rate of adenosine release into the extracellular milieu of the amygdala, cortex, or hippocampus is unlikely to be a marker of such a process.
dc.relation.isreferencedbyScopus
dc.titleExtracellular adenosine in the human brain during sleep and sleep deprivation: An in vivo microdialysis study
dc.typeArticle
dc.relation.ispartofjournalSleep
dc.relation.ispartofvolume29
dc.relation.ispartofissue4
dc.relation.ispartofpage455
dc.relation.ispartofpage461
dc.subject.keywordAdenosine; Amygdala; Circadian; Cortex; Epilepsy; Hippocampus; Human; Microdialysis; Sleep
dc.contributor.affiliationZeitzer, J.M., Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Stanford Center for Narcolepsy Research, Stanford University Medical Center, Palo Alto, CA, United States; Morales-Villagran, A., Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Centro Universitario de Ciencias Biol�gocas y Agropecuarias, Universidad de Guadalajara, Jalisco, Mexico; Maidment, N.T., Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Neuropsychiatric Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States; Behnke, E.J., Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Division of Neurosurgery, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States; Ackerson, L.C., Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States; Lopez-Rodriguez, F., Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Neuropsychiatric Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States; Fried, I., Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Neuropsychiatric Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Division of Neurosurgery, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States; Engel Jr., J., Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Neuropsychiatric Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Department of Neurobiology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States; Wilson, C.L., Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Neuropsychiatric Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, Department of Neurology, RNRC, UCLA School of Medicine, 710 Westwood Plaza, Los Angeles, CA 90095, United States
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