Ivan Soltesz received his doctorate in Budapest and conducted postdoctoral research at universities at Oxford, London, Stanford and Dallas. He established his laboratory at the University of California, Irvine, in 1995. He became full Professor in 2003, and served as department Chair from 2006 to July 2015. He returned to Stanford in 2015 as the James R. Doty Professor of Neurosurgery and Neurosciences at Stanford University School of Medicine. His major research interest is focused on neuronal microcircuits, network oscillations, cannabinoid signaling and the mechanistic bases of circuit dysfunction in epilepsy.
His laboratory employs a combination of closely integrated experimental and theoretical techniques, including closed-loop in vivo optogenetics, paired patch clamp recordings, in vivo electrophysiological recordings from identified interneurons in awake mice, 2-photon imaging, machine learning-aided 3D video analysis of behavior, video-EEG recordings, behavioral approaches, and large-scale computational modeling methods using supercomputers. He is the author of a book on GABAergic microcircuits (Diversity in the Neuronal Machine, Oxford University Press), and editor of a book on Computational Neuroscience in Epilepsy (Academic Press/Elsevier). He co-founded the first Gordon Research Conference on the Mechanisms of neuronal synchronization and epilepsy, and taught for five years in the Ion Channels Course at Cold Springs Harbor. He has over 30 years of research experience, with over 20 years as a faculty involved in the training of graduate students (total of 16, 6 of them MD/PhDs) and postdoctoral fellows (20), many of whom received fellowship awards, K99 grants, joined prestigious residency programs and became independent faculty.

Academic Appointments

Administrative Appointments

  • Assistant Professor, University of California, Irvine (1995 - 1999)
  • Associate Professor, University of California, Irvine (1999 - 2003)
  • Professor, University of California, Irvine (2003 - 2015)
  • Chair of Anatomy & Neurobiology, University of California, Irvine (2006 - 2015)
  • Chancellor's Professor, University of California, Irvine (2011 - 2015)
  • James R Doty Professor of Neurosurgery and Neurosciences, Stanford University (2015 - Present)
  • Vice Chair, Neurosurgery, Stanford University (2015 - Present)

Honors & Awards

  • Athalie Clark Research Award, University of California, Irvine (2005)
  • Javits Neuroscience Investigator Award, NINDS-NIH (2005)
  • Michael Prize in Epilepsy Research, Stiftung Michael, Germany (2009)
  • Research Recognition Award, Basic Science, American Epilepsy Society (2011)
  • Foreign Member, Hungarian Academy of Sciences (2016)

Boards, Advisory Committees, Professional Organizations

  • Co-Chair, Founder, Gordon Research Conference on Mechanisms of Epilepsy and Neuronal Synchronization (2006 - 2006)
  • Chair, Basic Science Committee, American Epilepsy Society (2006 - 2009)
  • Associate Editor, Journal of Neuroscience (2007 - 2012)
  • Member, Editorial Board, Epilepsy Research (2008 - 2015)
  • Member, Scientific Advisory Board, Citizens United in Research in Epilepsy (CURE) (2009 - 2012)
  • Co-Chair, Grants and Fellowship Review Panel, Epilepsy Foundation (2010 - 2012)
  • Chair, Clinical Neuroplasticity and Neurotransmitters (CNNT) study section, NIH (2011 - 2013)
  • Member, Professional Advisory Board, Epilepsy Foundation (2011 - Present)
  • Member, Editorial Board, Experimental Neurology (2013 - Present)
  • Chair, Research recognition Awards Committee, American Epilepsy Society (2016 - Present)

Professional Education

  • Postdoc, UT Southwestern, Neuroscience (1994)
  • Postdoc, Stanford University, Neuroscience (1993)
  • Postdoc, Universite Laval, Neuroscience (1992)
  • Postdoc, University of London, Neuroscience (1991)
  • Postdoc, Oxford University, Neuroscience (1990)
  • Ph.D., Eotvos University, Budapest, Comparative Physiology (1989)
  • University Diploma, Eotvos University, Budapest, Biology (1988)


2017-18 Courses

Stanford Advisees


All Publications

  • Dentate gyrus mossy cells control spontaneous convulsive seizures and spatial memory Science Bui, A., et al 2018

    View details for DOI 10.1126/science.aan4074

  • Persistent nature of alterations in cognition and neuronal circuit excitability after exposure to simulated cosmic radiation in mice Exp Neurol Parihar, V., et al 2018
  • Single Bursts of Individual Granule Cells Functionally Rearrange Feedforward Inhibition Journal of Neuroscience Neubrandt, M., et al 2018
  • Seizing Control: From Current Treatments to Optogenetic Interventions in Epilepsy NEUROSCIENTIST Bui, A. D., Alexander, A., Soltesz, I. 2017; 23 (1): 68-81
  • Extended Interneuronal Network of the Dentate Gyrus Cell Rep Szabo, G., et al 2017
  • Hippocampal Dentate Mossy Cells Improve Their CV and Trk into the Limelight Neuron Milstein, A., Soltesz, I. 2017
  • Involvement of fast-spiking cells in ictal sequences during spontaneous seizures in rats with chronic temporal lobe epilepsy Brain Neumann, A., et al 2017
  • Interneuronal mechanisms of hippocampal theta oscillations in a full-scale model of the rodent CA1 circuit. eLife Bezaire, M. J., Raikov, I., Burk, K., Vyas, D., Soltesz, I. 2016; 5


    The hippocampal theta rhythm plays important roles in information processing; however, the mechanisms of its generation are not well understood. We developed a data-driven, supercomputer-based, full-scale (1:1) model of the rodent CA1 area and studied its interneurons during theta oscillations. Theta rhythm with phase-locked gamma oscillations and phase-preferential discharges of distinct interneuronal types spontaneously emerged from the isolated CA1 circuit without rhythmic inputs. Perturbation experiments identified parvalbumin-expressing interneurons and neurogliaform cells, as well as interneuronal diversity itself, as important factors in theta generation. These simulations reveal new insights into the spatiotemporal organization of the CA1 circuit during theta oscillations.

    View details for DOI 10.7554/eLife.18566

    View details for PubMedID 28009257

    View details for PubMedCentralID PMC5313080

  • Neurophysiology of space travel: energetic solar particles cause cell type-specific plasticity of neurotransmission. Brain structure & function Lee, S., Dudok, B., Parihar, V. K., Jung, K., Zöldi, M., Kang, Y., Maroso, M., Alexander, A. L., Nelson, G. A., Piomelli, D., Katona, I., Limoli, C. L., Soltesz, I. 2016: -?


    In the not too distant future, humankind will embark on one of its greatest adventures, the travel to distant planets. However, deep space travel is associated with an inevitable exposure to radiation fields. Space-relevant doses of protons elicit persistent disruptions in cognition and neuronal structure. However, whether space-relevant irradiation alters neurotransmission is unknown. Within the hippocampus, a brain region crucial for cognition, perisomatic inhibitory control of pyramidal cells (PCs) is supplied by two distinct cell types, the cannabinoid type 1 receptor (CB1)-expressing basket cells (CB1BCs) and parvalbumin (PV)-expressing interneurons (PVINs). Mice subjected to low-dose proton irradiation were analyzed using electrophysiological, biochemical and imaging techniques months after exposure. In irradiated mice, GABA release from CB1BCs onto PCs was dramatically increased. This effect was abolished by CB1 blockade, indicating that irradiation decreased CB1-dependent tonic inhibition of GABA release. These alterations in GABA release were accompanied by decreased levels of the major CB1 ligand 2-arachidonoylglycerol. In contrast, GABA release from PVINs was unchanged, and the excitatory connectivity from PCs to the interneurons also underwent cell type-specific alterations. These results demonstrate that energetic charged particles at space-relevant low doses elicit surprisingly selective long-term plasticity of synaptic microcircuits in the hippocampus. The magnitude and persistent nature of these alterations in synaptic function are consistent with the observed perturbations in cognitive performance after irradiation, while the high specificity of these changes indicates that it may be possible to develop targeted therapeutic interventions to decrease the risk of adverse events during interplanetary travel.

    View details for PubMedID 27905022

  • Target-selectivity of parvalbumin-positive interneurons in layer II of medial entorhinal cortex in normal and epileptic animals. Hippocampus Armstrong, C., Wang, J., Yeun Lee, S., Broderick, J., Bezaire, M. J., Lee, S., Soltesz, I. 2016; 26 (6): 779-793


    The medial entorhinal cortex layer II (MEClayerII ) is a brain region critical for spatial navigation and memory, and it also demonstrates a number of changes in patients with, and animal models of, temporal lobe epilepsy (TLE). Prior studies of GABAergic microcircuitry in MEClayerII revealed that cholecystokinin-containing basket cells (CCKBCs) select their targets on the basis of the long-range projection pattern of the postsynaptic principal cell. Specifically, CCKBCs largely avoid reelin-containing principal cells that form the perforant path to the ipsilateral dentate gyrus and preferentially innervate non-perforant path forming calbindin-containing principal cells. We investigated whether parvalbumin containing basket cells (PVBCs), the other major perisomatic targeting GABAergic cell population, demonstrate similar postsynaptic target selectivity as well. In addition, we tested the hypothesis that the functional or anatomic arrangement of circuit selectivity is disrupted in MEClayerII in chronic TLE, using the repeated low-dose kainate model in rats. In control animals, we found that PVBCs innervated both principal cell populations, but also had significant selectivity for calbindin-containing principal cells in MEClayerII . However, the magnitude of this preference was smaller than for CCKBCs. In addition, axonal tracing and paired recordings showed that individual PVBCs were capable of contacting both calbindin and reelin-containing principal cells. In chronically epileptic animals, we found that the intrinsic properties of the two principal cell populations, the GABAergic perisomatic bouton numbers, and selectivity of the CCKBCs and PVBCs remained remarkably constant in MEClayerII . However, miniature IPSC frequency was decreased in epilepsy, and paired recordings revealed the presence of direct excitatory connections between principal cells in the MEClayerII in epilepsy, which is unusual in normal adult MEClayerII . Taken together, these findings advance our knowledge about the organization of perisomatic inhibition both in control and in epileptic animals. © 2015 Wiley Periodicals, Inc.

    View details for DOI 10.1002/hipo.22559

    View details for PubMedID 26663222

  • Target-Selectivity of Parvalbumin-Positive Interneurons in Layer II of Medial Entorhinal Cortex in Normal and Epileptic Animals HIPPOCAMPUS Armstrong, C., Wang, J., Lee, S. Y., Broderick, J., Bezaire, M. J., Lee, S., Soltesz, I. 2016; 26 (6): 779-793

    View details for DOI 10.1002/hipo.22559

    View details for Web of Science ID 000383272000009

  • Hippogate: a break-in from entorhinal cortex. Nature neuroscience Alexander, A., Soltesz, I. 2016; 19 (4): 530-532

    View details for DOI 10.1038/nn.4253

    View details for PubMedID 26878673

  • Cannabinoid Control of Learning and Memory through HCN Channels NEURON Maroso, M., Szabo, G. G., Kim, H. K., Alexander, A., Bui, A. D., Lee, S., Lutz, B., Soltesz, I. 2016; 89 (5): 1059-1073


    The mechanisms underlying the effects of cannabinoids on cognitive processes are not understood. Here we show that cannabinoid type-1 receptors (CB1Rs) control hippocampal synaptic plasticity and spatial memory through the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels that underlie the h-current (Ih), a key regulator of dendritic excitability. The CB1R-HCN pathway, involving c-Jun-N-terminal kinases (JNKs), nitric oxide synthase, and intracellular cGMP, exerts a tonic enhancement of Ih selectively in pyramidal cells located in the superficial portion of the CA1 pyramidal cell layer, whereas it is absent from deep-layer cells. Activation of the CB1R-HCN pathway impairs dendritic integration of excitatory inputs, long-term potentiation (LTP), and spatial memory formation. Strikingly, pharmacological inhibition of Ih or genetic deletion of HCN1 abolishes CB1R-induced deficits in LTP and memory. These results demonstrate that the CB1R-Ih pathway in the hippocampus is obligatory for the action of cannabinoids on LTP and spatial memory formation.

    View details for DOI 10.1016/j.neuron.2016.01.023

    View details for Web of Science ID 000373565400017

    View details for PubMedID 26898775

    View details for PubMedCentralID PMC4777634

  • Organization and control of epileptic circuits in temporal lobe epilepsy. Progress in brain research Alexander, A., Maroso, M., Soltesz, I. 2016; 226: 127-154


    When studying the pathological mechanisms of epilepsy, there are a seemingly endless number of approaches from the ultrastructural level-receptor expression by EM-to the behavioral level-comorbid depression in behaving animals. Epilepsy is characterized as a disorder of recurrent seizures, which are defined as "a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain" (Fisher et al., 2005). Such abnormal activity typically does not occur in a single isolated neuron; rather, it results from pathological activity in large groups-or circuits-of neurons. Here we choose to focus on two aspects of aberrant circuits in temporal lobe epilepsy: their organization and potential mechanisms to control these pathological circuits. We also look at two scales: microcircuits, ie, the relationship between individual neurons or small groups of similar neurons, and macrocircuits, ie, the organization of large-scale brain regions. We begin by summarizing the large body of literature that describes the stereotypical anatomical changes in the temporal lobe-ie, the anatomical basis of alterations in microcircuitry. We then offer a brief introduction to graph theory and describe how this type of mathematical analysis, in combination with computational neuroscience techniques and using parameters obtained from experimental data, can be used to postulate how microcircuit alterations may lead to seizures. We then zoom out and look at the changes which are seen over large whole-brain networks in patients and animal models, and finally we look to the future.

    View details for DOI 10.1016/bs.pbr.2016.04.007

    View details for PubMedID 27323941

  • Brain State Is a Major Factor in Preseizure Hippocampal Network Activity and Influences Success of Seizure Intervention JOURNAL OF NEUROSCIENCE Ewell, L. A., Liang, L., Armstrong, C., Soltesz, I., Leutgeb, S., Leutgeb, J. K. 2015; 35 (47): 15635-15648
  • Pass-Through Code of Synaptic Integration. Neuron Szabo, G. G., Soltesz, I. 2015; 87 (6): 1124-1126


    How do the components of neuronal circuits collaborate to select combinations of synaptic inputs from multiple pathways? In this issue of Neuron, Milstein et al. (2015) uncover mechanisms of synaptic facilitation and dendritic inhibition that cooperate to provide filtering for co-active inputs of distinct origins.

    View details for DOI 10.1016/j.neuron.2015.09.006

    View details for PubMedID 26402596

  • Regulation of fast-spiking basket cell synapses by the chloride channel ClC-2 NATURE NEUROSCIENCE Foldy, C., Lee, S., Morgan, R. J., Soltesz, I. 2010; 13 (9): 1047-1049


    Parvalbumin-expressing, fast-spiking basket cells are important for the generation of synchronous, rhythmic population activities in the hippocampus. We found that GABAA receptor-mediated synaptic inputs from murine parvalbumin-expressing basket cells were selectively modulated by the membrane voltage- and intracellular chloride-dependent chloride channel ClC-2. Our data reveal a previously unknown cell type-specific regulation of intracellular chloride homeostasis in the perisomatic region of hippocampal pyramidal neurons.

    View details for DOI 10.1038/nn.2609

    View details for Web of Science ID 000281332600006

    View details for PubMedID 20676104