
RESEARCH INTERESTS
Last Updated: 27 October 2020
My laboratory uses genetically-modified mice to study the roles that certain genes and gene products play in the presentation of abnormal neuroendocrine, neurological, and psychiatric responses. Traditionally, the identification of neuroendocrine dysfunction has involved biochemical analyses of hormonal responses, those for neurological disorders have relied upon behavioral and postmortem analyses, and those for psychiatric conditions have depended upon phenomenology. The use of genetic technologies has allowed specific genes in selected cells and in neural pathways to be related to certain molecular, biochemical, cellular, physiological, and behavioral dysfunctions. As the Director of the Mouse Behavioral and Neuroendocrine Analysis Core Facility at Duke University (http://sites.duke.edu/mousebehavioralcore/), we have phenotyped many different lines of inbred and mutant mice for my own work as well as for investigators at Duke and at other research institutions. As a consequence, we have helped to develop many different mouse genetic models of neuroendocrine and neuropsychiatric illness. We are working also with academic medicinal chemists and/or certain pharmacological/biotechnological companies to identify novel compounds that will ameliorate abnormal responses in various mutant mouse models. Some of these preclinical studies have formed a basis for clinical trials in humans.
Education and Training
- Massachusetts Institute of Technology, Ph.D. 1983
Selected Grants and Awards
- Exploiting Biased Agonism at the Ghrelin Receptor (GHSR 1a) for Opioid Addiction
- Evaluating cell type-specific non-dopaminergics as a Parkinson's treatment paradigm
- Interrogating the cholinergic basis of opioid reinforcement with subcellular precision
- Heat Shock Factors and Protein Misfolding Disease
- Phase 1 - Biased Agonists as Rapidly Acting Neuropsychiatric Drugs
- Neurovascular dysfunction in delirium superimposed on dementia
- Exploiting Dopamine Receptor Functional Selectivity as an Approach to Treat Parkinson's Symptoms
- Molecular and cellular control of injury-induced astrogenesis
- DART2.0: comprehensive cell type-specific behavioral neuropharmacology
- Targeting microbially-derived juvenile protective factors to resolve neuroinflammation and delirium
- Bioelectronic rescue of cognitive impairment after surgery
- In Vivo Epigenome Editing with CRISPR-Based Histone Acetyltransferase Transgenic Mice
- MECHANISTIC INSIGHTS INTO LSD ACTIONS AT 5-HT2A-SEROTONIN RECEPTORS
- Molecular and circuitry mechanism underlying autism behaviors in Shank3 mouse models
- Novel Adjuvants and Carriers for Opiod Vaccines
- Behavior and Physiology in Aging
- Developing a New Therapeutic Agent for Kabuki Syndrome
- Akt/GSK-3 Signaling Cascade and the Actions of Dopamine
- Simultaneous and Bidirectional Chemogenetic Control of Mesolimbic and Nigrostriatal Circuits
- Molecular, Synaptic, and Circuit Basis for Schizophrenia-related Phenotypes
- Developing a new therapeutic agent for Kabuki syndrome
- Molecular and circuitry mechanism underlying autism behaviors in Shank3 mouse models
- Cortico-striatal neurotransmission and compulsive motor behaviors
- Initial SHANK3 Study (Rugen E & F)
- Initial SHANK3 Study
- Linking Ciliary Biology to the Functional Annotation of Psychiatric Disorders
- Quantitative MR Microscopy of Phenotypic Biomarkers in Alzheimer's Disease
- Analysis of Shank3 Complete and Temporal and Spatial Specific Knockout Mice
- Receptor Regulation of CCK Cell Function
- IPA - Jiechun Zhou
- IPA - William Wetsel
- Fragile X Phenotypes Modulated by Altered Signaling to the Synaptic Cytoskeleton
- Linking ciliary biology to the functional annotation of psychiatric disorders
- Regulation of Cocaine Reward and Reinforcement by MeCP2
- Functional Selectivity: A Novel Approach for CNS Drug Discovery
- STIM1-dependent calcium signaling in neuronal responses to hypoxia and ischemia
- The 5-HT theory of depression tested in a naturalistic model of 5-HT deficiency
- Effect of two Rugen compounds on Novel Object Phobia in wild type (WT) and SAPAP3 KO mice
- Optimizing Lead 5-HT2C Ligands for Use in the Treatment of Schizoprenia
- Novel high-throughput screening for modifiers of TorsinA pathology
- Amphetamine-Induced Transcriptional Plasticity in Striatal GABAergic Interneurons
- Prevention of Temporal Lobe Epilepsy
- Regulation of response to chronic antidepressant treatment by MeCP2
- Imaging NFkB Activity in Relation to Animal Behavior in Peripheral Neuropathy
- Novel Genetic Mouse Model to Study the Consequences of TorsinA Dysfunction
- Non-invasive Chemical Genetic Control of Neuronal Activity
- Agilent Direct Drive 9.4T MRS/MRI Console
- PTSD-like phenotype of mice lacking GIT2
- Hormonal regulation of a Ca2+/AMPK signaling pathway
- Epigenetic regulation of transcriptional repression by drugs of abuse
- Stress and Behavior in Health and Disease
- Pharmacometabolomics Research Network
- Roles of SAPAP Proteins in Synaptic Function and Compulsive-like Behavior
- Cocaine Withdrawal: A Window of Treatment Opportunity
- Collaborative & Physiological Experiments to Breed CPE KO Mice
- The Pathophysiology of CMT2A in Cell and Animal Models
- Collaborative & Physiological Experiments to Breed CPE KO Mice
- Collaborative & Physiological Experiments
- Genetic Rescue Of Pro-Lhrh Processing In Cpefat Mice
- Collaborative & Physiological Experiments of CPE K/O Mice