Professional Education

  • Master of Science in Engr, E.S. Physiques Et Chimie Industrielles (2015)
  • Doctor of Science, Universite De Paris Vi (2019)
  • Licence, Universite de Paris V (Rene Descartes) (2013)
  • PhD, Sorbonne University, Paris, France, Neuroscience (2019)
  • Master, ESPCI & Paris Descartes University, France, Bioengineering and Innovation in Neurosciences (2015)
  • Bachelor, Paris Descartes University, France, Biomedical Sciences (2013)

Stanford Advisors

All Publications

  • Author Correction: Precise spatiotemporal control of voltage-gated sodium channels by photocaged saxitoxin. Nature communications Elleman, A. V., Devienne, G., Makinson, C. D., Haynes, A. L., Huguenard, J. R., Du Bois, J. 2022; 13 (1): 2277

    View details for DOI 10.1038/s41467-022-30054-8

    View details for PubMedID 35449160

  • Precise spatiotemporal control of voltage-gated sodium channels by photocaged saxitoxin. Nature communications Elleman, A. V., Devienne, G., Makinson, C. D., Haynes, A. L., Huguenard, J. R., Du Bois, J. 2021; 12 (1): 4171


    Here we report the pharmacologic blockade of voltage-gated sodium ion channels (NaVs) by a synthetic saxitoxin derivative affixed to a photocleavable protecting group. We demonstrate that a functionalized saxitoxin (STX-eac) enables exquisite spatiotemporal control of NaVs to interrupt action potentials in dissociated neurons and nerve fiber bundles. The photo-uncaged inhibitor (STX-ea) is a nanomolar potent, reversible binder of NaVs. We use STX-eac to reveal differential susceptibility of myelinated and unmyelinated axons in the corpus callosum to NaV-dependent alterations in action potential propagation, with unmyelinated axons preferentially showing reduced action potential fidelity under conditions of partial NaV block. These results validate STX-eac as a high precision tool for robust photocontrol of neuronal excitability and action potential generation.

    View details for DOI 10.1038/s41467-021-24392-2

    View details for PubMedID 34234116

  • Regulation of Perineuronal Nets in the Adult Cortex by the Activity of the Cortical Network JOURNAL OF NEUROSCIENCE Devienne, G., Picaud, S., Cohen, I., Piquet, J., Tricoire, L., Testa, D., Di Nardo, A. A., Rossier, J., Cauli, B., Lambolez, B. 2021; 41 (27): 5779-5790


    Perineuronal net (PNN) accumulation around parvalbumin-expressing (PV) inhibitory interneurons marks the closure of critical periods of high plasticity, whereas PNN removal reinstates juvenile plasticity in the adult cortex. Using targeted chemogenetic in vivo approaches in the adult mouse visual cortex, we found that transient inhibition of PV interneurons, through metabotropic or ionotropic chemogenetic tools, induced PNN regression. Electroencephalographic recordings indicated that inhibition of PV interneurons did not elicit unbalanced network excitation. Likewise, inhibition of local excitatory neurons also induced PNN regression, whereas chemogenetic excitation of either PV or excitatory neurons did not reduce the PNN. We also observed that chemogenetically inhibited PV interneurons exhibited reduced PNN compared to their untransduced neighbors, and confirmed that single PV interneurons express multiple genes enabling individual regulation of their own PNN density. Our results indicate that PNN density is regulated in the adult cortex by local changes of network activity that can be triggered by modulation of PV interneurons. PNN regulation may provide adult cortical circuits with an activity-dependent mechanism to control their local remodeling.SIGNIFICANCE STATEMENTThe perineuronal net is an extracellular matrix, which accumulates around individual parvalbumin-expressing inhibitory neurons during postnatal development, and is seen as a barrier that prevents plasticity of neuronal circuits in the adult cerebral cortex. We found that transiently inhibiting parvalbumin-expressing or excitatory cortical neurons triggers a local decrease of perineuronal net density. Our results indicate that perineuronal nets are regulated in the adult cortex depending on the activity of local microcircuits. These findings uncover an activity-dependent mechanism by which adult cortical circuits may locally control their plasticity.

    View details for DOI 10.1523/JNEUROSCI.0434-21.2021

    View details for Web of Science ID 000672106000002

    View details for PubMedID 34045309

    View details for PubMedCentralID PMC8265812

  • Single Cell Multiplex Reverse Transcription Polymerase Chain Reaction After Patch-clamp JOVE-JOURNAL OF VISUALIZED EXPERIMENTS Devienne, G., Le Gac, B., Piquet, J., Cauli, B. 2018


    The cerebral cortex is composed of numerous cell types exhibiting various morphological, physiological, and molecular features. This diversity hampers easy identification and characterization of these cell types, prerequisites to study their specific functions. This article describes the multiplex single cell reverse transcription polymerase chain reaction (RT-PCR) protocol, which allows, after patch-clamp recording in slices, to detect simultaneously the expression of tens of genes in a single cell. This simple method can be implemented with morphological characterization and is widely applicable to determine the phenotypic traits of various cell types and their particular cellular environment, such as in the vicinity of blood vessels. The principle of this protocol is to record a cell with the patch-clamp technique, to harvest and reverse transcribe its cytoplasmic content, and to detect qualitatively the expression of a predefined set of genes by multiplex PCR. It requires a careful design of PCR primers and intracellular patch-clamp solution compatible with RT-PCR. To ensure a selective and reliable transcript detection, this technique also requires appropriate controls from cytoplasm harvesting to amplification steps. Although precautions discussed here must be strictly followed, virtually any electrophysiological laboratory can use the multiplex single cell RT-PCR technique.

    View details for DOI 10.3791/57627

    View details for Web of Science ID 000444752100075

    View details for PubMedID 29985318

    View details for PubMedCentralID PMC6101963

  • Depdc5 knockdown causes mTOR-dependent motor hyperactivity in zebrafish ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY de Calbiac, H., Dabacan, A., Marsan, E., Tostivint, H., Devienne, G., Ishida, S., Leguern, E., Baulac, S., Muresan, R. C., Kabashi, E., Ciura, S. 2018; 5 (5): 510–23


    DEPDC5 was identified as a major genetic cause of focal epilepsy with deleterious mutations found in a wide range of inherited forms of focal epilepsy, associated with malformation of cortical development in certain cases. Identification of frameshift, truncation, and deletion mutations implicates haploinsufficiency of DEPDC5 in the etiology of focal epilepsy. DEPDC5 is a component of the GATOR1 complex, acting as a negative regulator of mTOR signaling.Zebrafish represents a vertebrate model suitable for genetic analysis and drug screening in epilepsy-related disorders. In this study, we defined the expression of depdc5 during development and established an epilepsy model with reduced Depdc5 expression.Here we report a zebrafish model of Depdc5 loss-of-function that displays a measurable behavioral phenotype, including hyperkinesia, circular swimming, and increased neuronal activity. These phenotypic features persisted throughout embryonic development and were significantly reduced upon treatment with the mTORC1 inhibitor, rapamycin, as well as overexpression of human WT DEPDC5 transcript. No phenotypic rescue was obtained upon expression of epilepsy-associated DEPDC5 mutations (p.Arg487* and p.Arg485Gln), indicating that these mutations cause a loss of function of the protein.This study demonstrates that Depdc5 knockdown leads to early-onset phenotypic features related to motor and neuronal hyperactivity. Restoration of phenotypic features by WT but not epilepsy-associated Depdc5 mutants, as well as by mTORC1 inhibition confirm the role of Depdc5 in the mTORC1-dependent molecular cascades, defining this pathway as a potential therapeutic target for DEPDC5-inherited forms of focal epilepsy.

    View details for DOI 10.1002/acn3.542

    View details for Web of Science ID 000431968300001

    View details for PubMedID 29761115

    View details for PubMedCentralID PMC5945968