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    Jeanne Paz, PhD

    TitleAssistant Professor
    SchoolUCSF School of Medicine
    DepartmentNeurology
    Address
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      Collapse Biography 
      Collapse Education and Training
      University Pierre et Marie CurieB.S.Cell Biology & Physiology2002
      University Pierre et Marie CurieM.S.Neuroscience2003
      University Pierre et Marie CuriePh.D.Neuroscience2007
      Stanford UniversityPostdocNeurology2012
      Stanford UniversityResearch AssociateNeurology and Bioengineering 2014
      Collapse Awards and Honors
      University Pierre and Marie Curie2002Undergraduate studentship Award (Bourse de mérite)
      University Pierre and Marie Curie2003 - 2005Teaching assistant grant (Monitorat)
      University Pierre and Marie Curie2003 - 2007Graduate Scholarship from the French Ministry of Research and Technology, Neuroscience program
      French Society for Neuroscience2005Award for the best poster presentation in Neuroscience
      French Society for Neuroscience, France2007Award for the best Neuroscience PhD thesis in France (“Prix de these”)
      University Pierre and Marie Curie2007Linus Pauling Graduate Scholar promotion
      French National Board of Universities2008Qualification to teach as Assistant Professor in any French University
      Jackson Laboratories 2011Award to attend “Coming Together on Epilepsy Genetics: From Human to Model Organisms and Back”
      CURE (Citizens United for Research in Epilepsy)2012Young investigator travel award to attend the Gordon Epilepsy Conference, Waterville
      NIH/NINDS2012K99/R00 Career Development Award
      CURE (Citizens United for Research in Epilepsy)2013Challenge Award
      Michael Foundation2015Michael Prize 2015

      Collapse Overview 
      Collapse Overview
      Our lab studies how neural synchronization and circuit plasticity relate to adaptive and maladaptive behavior. Our interests span many levels of analysis, from the cell to the circuit to animal behavior. The current major focus of our lab is epileptogenesis, the process by which a normal brain develops epilepsy. Our ultimate goal is to identify epilepsy control points in the brain and to develop strategies to prevent epileptogenesis.

      Epilepsy occurs in a number of neurological diseases. However, the underlying mechanisms of the condition are not well understood. While many antiepileptic drugs exist, they often have side effects and are unable to fully suppress the highly disruptive and potentially fatal symptoms seen in patients with epilepsy. We seek to improve this situation by investigating the cellular, circuit, and molecular mechanisms by which brain injuries, cerebrovascular disease, and genetic mutations cause epilepsy. In addition, we are exploring new strategies that predict seizures and block the pathogenic loops that can emerge between the cortical and subcortical brain regions in animal models of epilepsy. We combine bioengineering, engineering, neurophysiology and signal processing to achieve these goals. In particular, we are using optogenetic tools, which allow the control of specific elements of intact biological systems using light, to interrogate cells and synaptic components involved in adaptive and maladaptive neural circuit oscillations (i.e. epileptic seizure). We then couple these results with our in vitro findings to determine the cellular and microcircuit mechanisms that relate to these oscillations. After we identify the neural circuit that alleviates symptoms, we then target these circuits in the behaving animal at the onset of abnormal brain activity in real-time.

      Our work (Paz et al., Nature Neuroscience 2012) was the first to reveal that seizures can be instantaneously aborted in real-time with closed-loop optogenetic control of a specific cell type. This work led us to identify thalamocortical neurons as novel targets that control post-stroke seizures in real-time without side effects. We are currently adapting this approach to reveal control points in the brain—regions, cells, and circuits—in other forms of epilepsy and cognitive disorders.


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      Collapse Bibliographic 
      Collapse Publications
      Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Researchers can login to make corrections and additions, or contact us for help.
      List All   |   Timeline
      1. Lui H, Zhang J, Makinson SR, Cahill MK, Kelley KW, Huang HY, Shang Y, Oldham MC, Martens LH, Gao F, Coppola G, Sloan SA, Hsieh CL, Kim CC, Bigio EH, Weintraub S, Mesulam MM, Rademakers R, Mackenzie IR, Seeley WW, Karydas A, Miller BL, Borroni B, Ghidoni R, Farese RV, Paz JT, Barres BA, Huang EJ. Progranulin Deficiency Promotes Circuit-Specific Synaptic Pruning by Microglia via Complement Activation. Cell. 2016 May 5; 165(4):921-35. PMID: 27114033.
        View in: PubMed
      2. Hiu T, Farzampour Z, Paz JT, Wang EH, Badgely C, Olson A, Micheva KD, Wang G, Lemmens R, Tran KV, Nishiyama Y, Liang X, Hamilton SA, O'Rourke N, Smith SJ, Huguenard JR, Bliss TM, Steinberg GK. Enhanced phasic GABA inhibition during the repair phase of stroke: a novel therapeutic target. Brain. 2016 Feb; 139(Pt 2):468-80. PMID: 26685158.
        View in: PubMed
      3. Paz JT, Huguenard JR. Microcircuits and their interactions in epilepsy: is the focus out of focus? Nat Neurosci. 2015 Mar; 18(3):351-9. PMID: 25710837; PMCID: PMC4561622.
      4. Paz JT, Huguenard JR. Optogenetics and epilepsy: past, present and future. Epilepsy Curr. 2015 Jan-Feb; 15(1):34-8. PMID: 25678887; PMCID: PMC4320957.
      5. Paz JT, Davidson TJ, Frechette ES, Delord B, Parada I, Peng K, Deisseroth K, Huguenard JR. Closed-loop optogenetic control of thalamus as a tool for interrupting seizures after cortical injury. Nat Neurosci. 2013 Jan; 16(1):64-70. PMID: 23143518; PMCID: PMC3700812.
      6. Paz JT, Huguenard JR. R U OK? The Novel Therapeutic Potential of R Channels in Epilepsy. Epilepsy Curr. 2012 Mar; 12(2):75-6. PMID: 22473549; PMCID: PMC3316366.
      7. Naudé J, Paz JT, Berry H, Delord B. A theory of rate coding control by intrinsic plasticity effects. PLoS Comput Biol. 2012 Jan; 8(1):e1002349. PMID: 22275858; PMCID: PMC3261921.
      8. Paz JT, Bryant AS, Peng K, Fenno L, Yizhar O, Frankel WN, Deisseroth K, Huguenard JR. A new mode of corticothalamic transmission revealed in the Gria4(-/-) model of absence epilepsy. Nat Neurosci. 2011 Sep; 14(9):1167-73. PMID: 21857658; PMCID: PMC3308017.
      9. Yizhar O, Fenno LE, Prigge M, Schneider F, Davidson TJ, O'Shea DJ, Sohal VS, Goshen I, Finkelstein J, Paz JT, Stehfest K, Fudim R, Ramakrishnan C, Huguenard JR, Hegemann P, Deisseroth K. Neocortical excitation/inhibition balance in information processing and social dysfunction. Nature. 2011 Sep 8; 477(7363):171-8. PMID: 21796121; PMCID: PMC4155501.
      10. Paz JT, Christian CA, Parada I, Prince DA, Huguenard JR. Focal cortical infarcts alter intrinsic excitability and synaptic excitation in the reticular thalamic nucleus. J Neurosci. 2010 Apr 14; 30(15):5465-79. PMID: 20392967; PMCID: PMC2861582.
      11. Paz JT, Mahon S, Tiret P, Genet S, Delord B, Charpier S. Multiple forms of activity-dependent intrinsic plasticity in layer V cortical neurones in vivo. J Physiol. 2009 Jul 1; 587(Pt 13):3189-205. PMID: 19433575; PMCID: PMC2727031.
      12. Paz JT, Chavez M, Saillet S, Deniau JM, Charpier S. Activity of ventral medial thalamic neurons during absence seizures and modulation of cortical paroxysms by the nigrothalamic pathway. J Neurosci. 2007 Jan 24; 27(4):929-41. PMID: 17251435.
        View in: PubMed
      13. Paz JT, Deniau JM, Charpier S. Rhythmic bursting in the cortico-subthalamo-pallidal network during spontaneous genetically determined spike and wave discharges. J Neurosci. 2005 Feb 23; 25(8):2092-101. PMID: 15728849.
        View in: PubMed
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