Honors & Awards

  • NIMH Director's BRAINS Award, National Institute of Mental Health (2015-2020)
  • Baxter Faculty Scholar Award, Baxter Foundation (2015-2016)
  • MQ Fellow Award for Transforming Mental Health, MQ Foundation, London (2014-2017)
  • NARSAD Young Investigator Award, Brain & Behavior Research Foundation (2013-2015)
  • Alumni Excellence Research Award, Medicalis (2013)
  • Grand Prize Best Romanian Student Abroad, LRSA (2013)
  • Sammy Kuo Award, Best Postdoctoral publication in Neuroscience at Stanford University (2012)
  • Best Postdoctoral Research Award, Stanford University (2012)
  • Tashia & John Morgridge Endowed Fellow, Child Health Research Institute (CHRI) (2010-2012)
  • IBRO Outstanding Research Fellow, International Research Organization (IBRO) (2009-2010)
  • Scientific Achievements Prize, British Medical Journal (Ro) (2007)
  • High Academic Achievements Prize, Hatieganu School of Medicine (2007)
  • Medical Student of the Year, VIP Foundation (2006)
  • Ursus Research Prize, Hatieganu School of Medicine (2006)

Professional Education

  • Postdoctoral, Stanford University School of Medicine, Neuroscience (2013)
  • Medical Doctor, Hatieganu School of Medicine, Romania, Medicine (2007)

Community and International Work

  • Working group: Translating Mechanisms to Treatments in Autism Spectrum Disorders

    Ongoing Project


    Opportunities for Student Involvement


  • Lecturer in the Cold Spring Harbor Course in Autism Spectrum Disorders

    Ongoing Project


    Opportunities for Student Involvement


Research & Scholarship

Current Research and Scholarly Interests

Our lab is interested in deciphering the molecular and cellular mechanisms of neuropsychiatric disorders. To achieve this, we employ a multidisciplinary approach involving human genetics, molecular and developmental neurobiology, rodent disease models and neural cells differentiated from patient-derived induced pluripotent stem cells. We are also developing methods for generating specific classes of neurons from human stem cells and state-of-the-art tools for probing disease-relevant cellular endophenotypes. Our ultimate objective is to identify novel and reliable drug targets for neuropsychiatric disorders.


Journal Articles

  • Functional cortical neurons and astrocytes from human pluripotent stem cells in 3D cultures. Nature Methods Pasca, A. M., Sloan, S., Clarke, L. E., Tian, Y., Makinson, C., Huber, N., Kim, C., Park, J., O’Rourke, N., Nguyen, K., Smith, S. J., Huguenard, J., Geschwind, D. H., Barres, B. A., Pasca, S. P. 2015

    View details for DOI 10.1038/nmeth.3415

  • Generating human neurons in vitro and using them to understand neuropsychiatric disease. Annual Review of Neuroscience Pasca, S. P., Panagiotakos, G., Dolmetsch, R. 2014; 37: 479-501
  • Timothy syndrome is associated with activity-dependent dendritic retraction in rodent and human neurons NATURE NEUROSCIENCE Krey, J. F., Pasca, S. P., Shcheglovitov, A., Yazawa, M., Schwemberger, R., Rasmusson, R., Dolmetsch, R. E. 2013; 16 (2): 201-209


    L-type voltage gated calcium channels have an important role in neuronal development by promoting dendritic growth and arborization. A point mutation in the gene encoding Ca(V)1.2 causes Timothy syndrome, a neurodevelopmental disorder associated with autism spectrum disorders (ASDs). We report that channels with the Timothy syndrome alteration cause activity-dependent dendrite retraction in rat and mouse neurons and in induced pluripotent stem cell (iPSC)-derived neurons from individuals with Timothy syndrome. Dendrite retraction was independent of calcium permeation through the mutant channel, was associated with ectopic activation of RhoA and was inhibited by overexpression of the channel-associated GTPase Gem. These results suggest that Ca(V)1.2 can activate RhoA signaling independently of Ca(2+) and provide insights into the cellular basis of Timothy syndrome and other ASDs.

    View details for DOI 10.1038/nn.3307

    View details for Web of Science ID 000314260200017

    View details for PubMedID 23313911

  • Using iPSC-derived neurons to uncover cellular phenotypes associated with Timothy syndrome NATURE MEDICINE Pasca, S. P., Portmann, T., Voineagu, I., Yazawa, M., Shcheglovitov, A., Pasca, A. M., Cord, B., Palmer, T. D., Chikahisa, S., Nishino, S., Bernstein, J. A., Hallmayer, J., Geschwind, D. H., Dolmetsch, R. E. 2011; 17 (12): 1657-U176


    Monogenic neurodevelopmental disorders provide key insights into the pathogenesis of disease and help us understand how specific genes control the development of the human brain. Timothy syndrome is caused by a missense mutation in the L-type calcium channel Ca(v)1.2 that is associated with developmental delay and autism. We generated cortical neuronal precursor cells and neurons from induced pluripotent stem cells derived from individuals with Timothy syndrome. Cells from these individuals have defects in calcium (Ca(2+)) signaling and activity-dependent gene expression. They also show abnormalities in differentiation, including decreased expression of genes that are expressed in lower cortical layers and in callosal projection neurons. In addition, neurons derived from individuals with Timothy syndrome show abnormal expression of tyrosine hydroxylase and increased production of norepinephrine and dopamine. This phenotype can be reversed by treatment with roscovitine, a cyclin-dependent kinase inhibitor and atypical L-type-channel blocker. These findings provide strong evidence that Ca(v)1.2 regulates the differentiation of cortical neurons in humans and offer new insights into the causes of autism in individuals with Timothy syndrome.

    View details for DOI 10.1038/nm.2576

    View details for Web of Science ID 000297978000039

    View details for PubMedID 22120178

  • Alteration in basal and depolarization induced transcriptional network in iPSC derived neurons fromTimothy syndrome Genome Medicine Tian, Y., Voineagu, I., Pasca, S. P., Won, H., Chandran, V., Horvath, S., Dolmetsch, R. E., Geschwind, D. H. 2014; 6 (75)
  • A promoter in the coding region of the calcium channel gene CACNA1C generates the transcription factor CCAT. PloS one Gomez-Ospina, N., Panagiotakos, G., Portmann, T., Pasca, S. P., Rabah, D., Budzillo, A., Kinet, J. P., Dolmetsch, R. E. 2013; 8 (4)


    The C-terminus of the voltage-gated calcium channel Cav1.2 encodes a transcription factor, the calcium channel associated transcriptional regulator (CCAT), that regulates neurite extension and inhibits Cav1.2 expression. The mechanisms by which CCAT is generated in neurons and myocytes are poorly understood. Here we show that CCAT is produced by activation of a cryptic promoter in exon 46 of CACNA1C, the gene that encodes CaV1.2. Expression of CCAT is independent of Cav1.2 expression in neuroblastoma cells, in mice, and in human neurons derived from induced pluripotent stem cells (iPSCs), providing strong evidence that CCAT is not generated by cleavage of CaV1.2. Analysis of the transcriptional start sites in CACNA1C and immune-blotting for channel proteins indicate that multiple proteins are generated from the 3' end of the CACNA1C gene. This study provides new insights into the regulation of CACNA1C, and provides an example of how exonic promoters contribute to the complexity of mammalian genomes.

    View details for DOI 10.1371/journal.pone.0060526

    View details for PubMedID 23613729

  • Motor abnormalities as a putative endophenotype for Autism Spectrum Disorders. Frontiers in integrative neuroscience Esposito, G., Pasca, S. P. 2013; 7: 43-?


    Autism Spectrum Disorders (ASDs) represent a complex group of behaviorally defined conditions with core deficits in social communication and the presence of repetitive and restrictive behaviors. To date, neuropathological studies have failed to identify pathognomonic cellular features for ASDs and there remains a fundamental disconnection between the complex clinical aspects of ASDs and the underlying neurobiology. Although not listed among the core diagnostic domains of impairment in ASDs, motor abnormalities have been consistently reported across the spectrum. In this perspective article, we summarize the evidence that supports the use of motor abnormalities as a putative endophenotype for ASDs. We argue that because these motor abnormalities do not directly depend on social or linguistic development, they may serve as an early disease indicator. Furthermore, we propose that stratifying patients based on motor development could be useful not only as an outcome predictor and in identifying more specific treatments for different ASDs categories, but also in exposing neurobiological mechanisms.

    View details for DOI 10.3389/fnint.2013.00043

    View details for PubMedID 23781177

  • Surround modulation of neuronal responses in V1 is as stable over time as responses to direct stimulation of receptive fields. Cortex Pasca SP, Singer W, Nikolic D 2010; 46 (9): 1199-203
  • Paraoxonase 1 activities and polymorphisms in autism spectrum disorders. Journal of Cellular and Molecular Medicine Pasca, S., Dronca E, Nemes B; B, Kaucsr T, Endreffy E, Iftene F, Benga I, Cornean R, Dronca M. 2010; 14 (3): 600-7
  • One carbon metabolism disturbances and the C677T MTHFR gene polymorphism in children with autism spectrum disorders. Journal of Cellular and Molecular Medicine Pasca, S., Dronca E, Kaucsr T, Craciun EC, Endreffy E, Ferencz BK, Iftene F, Benga I, Cornean R, Banerjee R, Dronca M. 2009; 13 (10): 4229-38
  • Serum paraoxonase 1 activities and homocysteinemia in hemodialysis patients. Clinical chemistry and laboratory medicine Dronca M, Pasca SP, Nemes B, Vlase L, Vladutiu D. 2008; 46 (6): 880-1
  • Vomiting is not an adaption for glaucoma (and Darwinian medicine is difficult). Medical Hypotheses Pasca SP, Nesse RM 2008; 71 (3): 472-3
  • High levels of homocysteine and low serum paraoxonase 1 arylesterase activity in children with autism. Life Sciences Pasca SP, Nemes B, Vlase L, Gagyi CE, Dronca E, Miu AC, Dronca M. 2006; 78 (19): 2244-48
  • Behavioral effects of corpus callosum transection and environmental enrichment in adult rats. Behavioural brain research Miu AC, Heilman RM, Pasca SP, Stefan CA, Spânu F, Vasiu R, Olteanu AI, Miclea M. 2006; 172 (1): 135-44

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