Alicia Y Che, PhD
Cards
Appointments
Titles
Director of Graduate Admissions, Interdepartmental Neuroscience Program
Contact Info
Appointments
Titles
Director of Graduate Admissions, Interdepartmental Neuroscience Program
Contact Info
Appointments
Titles
Director of Graduate Admissions, Interdepartmental Neuroscience Program
Contact Info
About
Titles
Assistant Professor of Psychiatry
Director of Graduate Admissions, Interdepartmental Neuroscience ProgramBiography
Dr. Che joined the faculty of Yale Department of Psychiatry in 2021, after completing her postdoctoral fellowship with Dr. Natalia De Marco García at Weill Cornell Medical College and Dr. Gord Fishell at NYU. She earned a Ph.D. in Physiology and Neurobiology in the laboratory of Dr. Joseph LoTurco at the University of Connecticut in 2014. She received a B.S. triple-majoring in Biology, Physics and Physical Chemistry at Pacific Lutheran University in Washington state in 2009.
Appointments
Psychiatry
Assistant ProfessorPrimary
Other Departments & Organizations
- Center for Brain & Mind Health
- Interdepartmental Neuroscience Program
- Janeway Society
- Neural Disorders
- Neuroscience Research Training Program (NRTP)
- Neuroscience Track
- Psychiatry
- Yale Center for the Science of Cannabis and Cannabinoids
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
Education & Training
- PhD
- University of Connecticut, Physiology and Neurobiology (2014)
- BS
- Pacific Lutheran University, Biology, Physics, Physical Chemistry (2009)
Research
Overview
Project 1. The Role of Oxytocin on the Development of Social Behavior
Touch contributes powerfully to parent-infant interactions that are fundamental for early social behavior development. Abnormalities in tactile perception are prevalent features in individuals with autism spectrum disorders (ASD), exacerbating the core social deficits. While the neural mechanisms underlying the interplay between tactile input and social behavior is not yet known, a prominent route through which social information can be conveyed to neurons is oxytocin signaling. In neurons, oxytocin modulates inhibition to increase signal-to-noise ratios, promote long-term synaptic plasticity, and enhance the salience of socially-relevant stimuli. We are investigating how oxytocin facilitates the development of social touch on a circuit level. We use a combination of techniques including mouse genetics, slice electrophysiology, longitudinal in vivo 2-photon imaging on behaving animals to reveal how circuits underlying whisker-dependent social interaction is established.
Project 2. Circuit Dysfunction in PTSD
PTSD is a debilitating disorder involving intrusive memories of a traumatic events, which are due in part to an inability to modify responses to stimuli that are no longer threatening – a process known as extinction. The medial prefrontal cortex (mPFC) plays a critical role in extinction, however the circuit-level mechanisms that support extinction learning in the mPFC are not completely understood. Recent TWAS and gene expression studies on PTSD postmortem brain revealed numerous dysregulated genes expressed in GABAergic neurons in the dlPFC that are also key drivers capable of coordinating transcriptomic organization. We aim to understand how these genes are involved in fear extinction on cellular, circuit and functional levels with an emphasis on the developmental period, leveraging new technologies for cell type-specific genetic manipulations and 2-photon imaging through chronically implanted microprisms.
Research at a Glance
Publications Timeline
Publications
2023
Neural Circuit Transitions Supporting Developmentally Specific Social Behavior.
Ferrara NC, Che A, Briones B, Padilla-Coreano N, Lovett-Barron M, Opendak M. Neural Circuit Transitions Supporting Developmentally Specific Social Behavior. J Neurosci 2023, 43: 7456-7462. PMID: 37940586, DOI: 10.1523/JNEUROSCI.1377-23.2023.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements
2021
An in vivo Calcium Imaging Approach for the Identification of Cell-Type Specific Patterns in the Developing Cortex.
Che A, De Marco García NV. An in vivo Calcium Imaging Approach for the Identification of Cell-Type Specific Patterns in the Developing Cortex. Frontiers In Neural Circuits 2021, 15: 747724. PMID: 34690708, PMCID: PMC8528153, DOI: 10.3389/fncir.2021.747724.Peer-Reviewed Original Research
2020
The epichaperome is a mediator of toxic hippocampal stress and leads to protein connectivity-based dysfunction
Inda MC, Joshi S, Wang T, Bolaender A, Gandu S, Koren III J, Che AY, Taldone T, Yan P, Sun W, Uddin M, Panchal P, Riolo M, Shah S, Barlas A, Xu K, Chan LYL, Gruzinova A, Kishinevsky S, Studer L, Fossati V, Noggle SA, White JR, de Stanchina E, Sequeira S, Anthoney KH, Steele JW, Manova-Todorova K, Patil S, Dunphy MP, Pillarsetty N, Pereira AC, Erdjument-Bromage H, Neubert TA, Rodina A, Ginsberg SD, De Marco Garcia N, Luo W, Chiosis G. The epichaperome is a mediator of toxic hippocampal stress and leads to protein connectivity-based dysfunction. Nature Communications 2020, 11: 319. PMID: 31949159, PMCID: PMC6965647, DOI: 10.1038/s41467-019-14082-5.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsAssemblies of Perisomatic GABAergic Neurons in the Developing Barrel Cortex.
Modol L, Bollmann Y, Tressard T, Baude A, Che A, Duan ZRS, Babij R, De Marco García NV, Cossart R. Assemblies of Perisomatic GABAergic Neurons in the Developing Barrel Cortex. Neuron 2020, 105: 93-105.e4. PMID: 31780328, PMCID: PMC7537946, DOI: 10.1016/j.neuron.2019.10.007.Peer-Reviewed Original ResearchGABAergic Restriction of Network Dynamics Regulates Interneuron Survival in the Developing Cortex.
Duan ZRS, Che A, Chu P, Modol L, Bollmann Y, Babij R, Fetcho RN, Otsuka T, Fuccillo MV, Liston C, Pisapia DJ, Cossart R, De Marco García NV. GABAergic Restriction of Network Dynamics Regulates Interneuron Survival in the Developing Cortex. Neuron 2020, 105: 75-92.e5. PMID: 31780329, PMCID: PMC6982374, DOI: 10.1016/j.neuron.2019.10.008.Peer-Reviewed Original Research
2018
Layer I Interneurons Sharpen Sensory Maps during Neonatal Development.
Che A, Babij R, Iannone AF, Fetcho RN, Ferrer M, Liston C, Fishell G, De Marco García NV. Layer I Interneurons Sharpen Sensory Maps during Neonatal Development. Neuron 2018, 99: 98-116.e7. PMID: 29937280, PMCID: PMC6152945, DOI: 10.1016/j.neuron.2018.06.002.Peer-Reviewed Original Research
2017
Rescue of impaired sociability and anxiety-like behavior in adult cacna1c-deficient mice by pharmacologically targeting eIF2α.
Kabir ZD, Che A, Fischer DK, Rice RC, Rizzo BK, Byrne M, Glass MJ, De Marco Garcia NV, Rajadhyaksha AM. Rescue of impaired sociability and anxiety-like behavior in adult cacna1c-deficient mice by pharmacologically targeting eIF2α. Molecular Psychiatry 2017, 22: 1096-1109. PMID: 28584287, PMCID: PMC5863913, DOI: 10.1038/mp.2017.124.Peer-Reviewed Original Research
2015
Tracking and transforming neocortical progenitors by CRISPR/Cas9 gene targeting and piggyBac transposase lineage labeling.
Chen F, Rosiene J, Che A, Becker A, LoTurco J. Tracking and transforming neocortical progenitors by CRISPR/Cas9 gene targeting and piggyBac transposase lineage labeling. Development (Cambridge, England) 2015, 142: 3601-11. PMID: 26400094, PMCID: PMC4631763, DOI: 10.1242/dev.118836.Peer-Reviewed Original ResearchMutation of the Dyslexia-Associated Gene Dcdc2 Enhances Glutamatergic Synaptic Transmission Between Layer 4 Neurons in Mouse Neocortex.
Che A, Truong DT, Fitch RH, LoTurco JJ. Mutation of the Dyslexia-Associated Gene Dcdc2 Enhances Glutamatergic Synaptic Transmission Between Layer 4 Neurons in Mouse Neocortex. Cerebral Cortex 2015, 26: 3705-3718. PMID: 26250775, PMCID: PMC5004750, DOI: 10.1093/cercor/bhv168.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsN-methyl-D-aspartate receptor antagonistFunctional synaptic circuitryEvoked glutamate releaseGlutamatergic synaptic transmissionLayer 4 neuronsExcitatory transmissionGlutamate releaseThalamocortical connectionsAmbient glutamateMK-801Receptor antagonistAcute applicationProbability of releaseSomatosensory cortexSynaptic circuitryNMDAR activationSynaptic transmissionSynaptic releaseExcitatory connectivityPostsynaptic NMDARsCortical connectivitySomatosensory neocortexMouse neocortexNMDARNeocortex
2014
DCDC2 Mutations Cause a Renal-Hepatic Ciliopathy by Disrupting Wnt Signaling
Schueler M, Braun DA, Chandrasekar G, Gee HY, Klasson TD, Halbritter J, Bieder A, Porath JD, Airik R, Zhou W, LoTurco JJ, Che A, Otto EA, Böckenhauer D, Sebire NJ, Honzik T, Harris PC, Koon SJ, Gunay-Aygun M, Saunier S, Zerres K, Bruechle NO, Drenth JP, Pelletier L, Tapia-Páez I, Lifton RP, Giles RH, Kere J, Hildebrandt F. DCDC2 Mutations Cause a Renal-Hepatic Ciliopathy by Disrupting Wnt Signaling. American Journal Of Human Genetics 2014, 96: 81-92. PMID: 25557784, PMCID: PMC4289677, DOI: 10.1016/j.ajhg.2014.12.002.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsBeta CateninCiliaComputational BiologyDishevelled ProteinsExonsHEK293 CellsHumansKidneyKidney Diseases, CysticMiceMicroscopy, Electron, TransmissionMicrotubule-Associated ProteinsMutationNIH 3T3 CellsPhenotypePhosphoproteinsWnt Signaling PathwayZebrafishConceptsNPHP-RCWnt inhibitorsΒ-catenin-dependent WntMitotic spindle fibersImportance of WntCiliary axonemeHuman mutationsRenal tubulogenesisWntCiliopathiesSpindle fibersCiliogenesisMutationsDCDC2Dependent mannerKnockdownCentral roleRecessive diseaseInhibitorsMutantsDCDC2 mutationsTubulogenesisAxonemePhenotypeDvl
Academic Achievements and Community Involvement
honor NARSAD Young Investigator Award
International AwardBrain & Behavior Research FoundationDetails01/13/2020United Stateshonor K99/R00 Pathway to Independence Award
National AwardNINDSDetails12/09/2019United States
Links & Media
Get In Touch
Contacts
Locations
Connecticut Mental Health Center
Academic Office
34 Park Street, Rm W215
New Haven, CT 06519