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Signaling events in activity dependent neuroprotection, neurodegeneration, and synaptic plasticity

Lee, Bo Young
http://rave.ohiolink.edu/etdc/view?acc_num=osu1180458484

Abstract Details

2007, Doctor of Philosophy, Ohio State University, Neuroscience.
CREB-(cAMP response element binding protein) dependent gene transcription within the context of physiological and patho-physiological conditions is a central focus of my dissertation. CREB is a transcription factor that plays a role in many activity-dependent neuronal processes, such as learning and memory, neuroprotection and neurotransmission. Initially, in chapter 1, I examined cellular and molecular signaling events that couple excitotoxic and nontoxic levels of NMDA receptor stimulation to activation of the CREB/cAMP response element (CRE) pathway in cultured cortical neurons. In this study, I report that the temporal regulation of CREB activation is an essential cue that controls the efficacy of NMDA as a regulator of CRE-mediated transcription. In chapter 2, I examined the role of the CREB/CRE-dependent signaling pathway under pathological conditions elicited by status epilepticus (SE). First, to characterize how seizure activity regulates the activation state of the CREB/CRE pathway in both glia and neurons of the hippocampus. I found that SE triggers two waves of CREB-mediated gene expression, a transient wave in neurons and a long-lasting wave in reactive glial cells, and that CREB couples SE to COX-2 expression. In chapter 3, I examined the role of the CREB/CRE pathway as a signaling intermediate that couples a BDNF-evoked preconditioning stimulus to protection against SE-induced neuronal death in the striatum. I found that SE evoked cell deaths were dramatically attenuated by BDNF infusion directly into striatum 24 hr prior to SE. I found MAPK-CREB transcription pathway is essential for BDNF mediated neuroprotection and one of CREB target genes, PGC-1 alpha may play a role in this BDNF mediated neuroprotection through CREB transcription signaling pathway. In chapter 4, I redirected my focus on the analysis of signaling pathways that couple excitatory neurotransmission to entrainment of the circadian clock. The mammalian circadian pacemaker located in the suprachiasmatic nuclei (SCN) drives a vast array of biochemical and physiological processes with 24 hr periodicity. I examined the role of protein kinase C (PKC) in clock entrainment. I found that PKC may influence clock entrainment via posttranslational mechanisms that influence clock protein stability.
Karl Obrietan (Advisor)

Recommended Citations

Citations

  • Lee, B. Y. (2007). Signaling events in activity dependent neuroprotection, neurodegeneration, and synaptic plasticity [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1180458484

    APA Style (7th edition)

  • Lee, Bo Young. Signaling events in activity dependent neuroprotection, neurodegeneration, and synaptic plasticity. 2007. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1180458484.

    MLA Style (8th edition)

  • Lee, Bo Young. "Signaling events in activity dependent neuroprotection, neurodegeneration, and synaptic plasticity." Doctoral dissertation, Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=osu1180458484

    Chicago Manual of Style (17th edition)

osu1180458484
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© 2007, all rights reserved.
This open access ETD is published by The Ohio State University and OhioLINK.