I am a postdoctoral fellow interested in using multiplexing molecular, electrophysiological, and microscopy techniques to
dissect the function of brain circuits in health and disease

Honors & Awards

  • NIH Ruth L. Kirschstein National Research Service Award (F32), NIAAA (2020)
  • Featured Microscopy Image, "Beautiful Brain Exhibit", Ackland Art Museum (2019)
  • Cover Art, Genes, Brain, and Behavior (2018)
  • NIH Ruth L. Kirschstein National Research Service Award (F31), NIAAA (2017)
  • Outstanding Undergraduate Thesis Award, Phi Beta Kappa (2014)
  • PIRE Fellow, National Science Foundation (2013)

Boards, Advisory Committees, Professional Organizations

  • Member, Society for Neuroscience (2014 - Present)
  • Member, Research Society on Alcoholism (2017 - Present)

Professional Education

  • PhD, The University of North Carolina at Chapel Hill, Neuroscience (2019)
  • BS, The Pennsylvania State University, Biology (2014)

Stanford Advisors

  • Jun Ding, Postdoctoral Faculty Sponsor


All Publications

  • Central Amygdala Prepronociceptin-Expressing Neurons Mediate Palatable Food Consumption and Reward NEURON Hardaway, J., Halladay, L. R., Mazzone, C. M., Pati, D., Bloodgood, D. W., Kim, M., Jensen, J., DiBerto, J. F., Boyt, K. M., Shiddapur, A., Erfani, A., Hon, O. J., Neira, S., Stanhope, C. M., Sugam, J. A., Saddoris, M. P., Tipton, G., McElligott, Z., Jhou, T. C., Stuber, G. D., Bruchas, M. R., Bulik, C. M., Holmes, A., Kash, T. L. 2019; 102 (5): 1037-+


    Food palatability is one of many factors that drives food consumption, and the hedonic drive to feed is a key contributor to obesity and binge eating. In this study, we identified a population of prepronociceptin-expressing cells in the central amygdala (PnocCeA) that are activated by palatable food consumption. Ablation or chemogenetic inhibition of these cells reduces palatable food consumption. Additionally, ablation of PnocCeA cells reduces high-fat-diet-driven increases in bodyweight and adiposity. PnocCeA neurons project to the ventral bed nucleus of the stria terminalis (vBNST), parabrachial nucleus (PBN), and nucleus of the solitary tract (NTS), and activation of cell bodies in the central amygdala (CeA) or axons in the vBNST, PBN, and NTS produces reward behavior but did not promote feeding of palatable food. These data suggest that the PnocCeA network is necessary for promoting the reinforcing and rewarding properties of palatable food, but activation of this network itself is not sufficient to promote feeding.

    View details for DOI 10.1016/j.neuron.2019.03.037

    View details for Web of Science ID 000470104900015

    View details for PubMedID 31029403

    View details for PubMedCentralID PMC6750705

  • Dynorphin-kappa opioid receptor activity in the central amygdala modulates binge-like alcohol drinking in mice NEUROPSYCHOPHARMACOLOGY Anderson, R. I., Lopez, M. F., Griffin, W. C., Haun, H. L., Bloodgood, D. W., Pati, D., Boyt, K. M., Kash, T. L., Becker, H. C. 2019; 44 (6): 1084-1092


    Although previous research has demonstrated a role for kappa opioid receptor-mediated signaling in escalated alcohol consumption associated with dependence and stress exposure, involvement of the dynorphin/kappa opioid receptor (DYN/KOR) system in binge-like drinking has not been fully explored. Here we used pharmacological and chemogenetic approaches to examine the influence of DYN/KOR signaling on alcohol consumption in the drinking-in-the-dark (DID) model of binge-like drinking. Systemic administration of the KOR agonist U50,488 increased binge-like drinking (Experiment 1) while, conversely, systemic administration of the KOR antagonist nor-BNI reduced drinking in the DID model (Experiment 2). These effects of systemic KOR manipulation were selective for alcohol as neither drug influenced consumption of sucrose in the DID paradigm (Experiment 3). In Experiment 4, administration of the long-acting KOR antagonist nor-BNI into the central nucleus of the amygdala (CeA) decreased alcohol intake. Next, targeted "silencing" of DYN+ neurons in the CeA was accomplished using a chemogenetic strategy. Cre-dependent viral expression in DYN+ neurons was confirmed in CeA of Pdyn-IRES-Cre mice and functionality of an inhibitory (hM4Di) DREADD was validated (Experiment 5). Activating the inhibitory DREADD by CNO injection reduced binge-like alcohol drinking, but CNO injection did not alter alcohol intake in mice that were treated with control virus (Experiment 6). Collectively, these results demonstrate that DYN/KOR signaling in the CeA contributes to excessive alcohol consumption in a binge-drinking model.

    View details for DOI 10.1038/s41386-018-0294-3

    View details for Web of Science ID 000464017300011

    View details for PubMedID 30555162

    View details for PubMedCentralID PMC6461883

  • Dynorphin Controls the Gain of an Amygdalar Anxiety Circuit CELL REPORTS Crowley, N. A., Bloodgood, D. W., Hardaway, J., Kendra, A. M., McCall, J. G., Al-Hasani, R., McCall, N. M., Yu, W., Schools, Z. L., Krashes, M. J., Lowell, B. B., Whistler, J. L., Bruchas, M. R., Kash, T. L. 2016; 14 (12): 2774-2783


    Kappa opioid receptors (KORs) are involved in a variety of aversive behavioral states, including anxiety. To date, a circuit-based mechanism for KOR-driven anxiety has not been described. Here, we show that activation of KORs inhibits glutamate release from basolateral amygdala (BLA) inputs to the bed nucleus of the stria terminalis (BNST) and occludes the anxiolytic phenotype seen with optogenetic activation of BLA-BNST projections. In addition, deletion of KORs from amygdala neurons results in an anxiolytic phenotype. Furthermore, we identify a frequency-dependent, optically evoked local dynorphin-induced heterosynaptic plasticity of glutamate inputs in the BNST. We also find that there is cell type specificity to the KOR modulation of the BLA-BNST input with greater KOR-mediated inhibition of BLA dynorphin-expressing neurons. Collectively, these results provide support for a model in which local dynorphin release can inhibit an anxiolytic pathway, providing a discrete therapeutic target for the treatment of anxiety disorders.

    View details for DOI 10.1016/j.celrep.2016.02.069

    View details for Web of Science ID 000372869300002

    View details for PubMedID 26997280

    View details for PubMedCentralID PMC4814306

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