Profile

Nigel S. Bamford, MD

Nigel S. Bamford, MD

Neurology

On staff since October 2002

Academic Title: Associate Professor of Neurology, Adjunct Associate Professor of Pediatrics and Psychology

Research Center: Center for Integrative Brain Research

Dr. Bamford sees patients in clinic and in hospital. His clinical focus is on movement disorders, but treats patients with a wide variety of neurological diseases and conditions. Dr. Bamford is an Attending on the Child Neurology Service at Seattle Childrens Hospital, where he supervises pediatric, neurology, neurosurgery, and psychiatry residents and medical students. Dr. Bamford also supervises child neurology residents in monthly four-hour outpatient continuity clinics. Dr. Bamford also spends time performing basic science research. He is funded though NIH, as well as by a number of private grants. Bamford also participates in clinical research and is a Co-PI on two clinical research trials; Berlin Heart clinical trial at Seattle Childrens Hospital, Seattle and the FHCRC clinical trial, A Pilot Study of High-Dose Immunosuppressive Therapy Using Carmustine, Etoposide, Cytarabine, and Melphalan (BEAM) + Thymoglobulin Followed by Syngeneic or Autologous Hematopoietic Cell Transplantation for Patients with Autoimmune Neurologic Diseases.

Dr. Bamford's basic science research focuses on function and regulation of striatal synaptic activity in the mammalian basal ganglia. The neostriatum plays an important role in cognition, voluntary movement and addiction. As such, evaluation of striatal function is paramount to understanding numerous developmental, neurological, and psychiatric disorders, including Tourette syndrome, attention deficit hyperactivity disorder, substance abuse, Parkinsons disease and Huntingtons disease. New treatments are needed and Bamfords investigations offer critical insights into novel treatment options.

Current laboratory investigations focus on the function of the mammalian corticostriatal system (the collection of neurons that connect the cerebral cortex and striatum) and its role in motor learning as well as the mechanisms underlying substance abuse, Parkinsons disease and Huntingtons disease. In these disorders, too much or too little dopamine is thought to alter striatal excitation, resulting in clinical symptoms. To gain insights into synaptic plasticity induced by alterations in dopamine availability, the Bamford Lab combine behavioral investigations with optical, electrophysiological, and immunohistochemical methods to observe the effects of dopamine and acetylcholine on glutamate release in the striatum. Bamford has published many high quality papers in Neuron, the Journal of Neuroscience, Annals of Neurology, and Nature Neuroscience. His work describes a newly developed technique that allows direct visualization and measurement of release from presynaptic cortical terminals within the striatum. These investigations demonstrate that glutamate release from cortical projections in the motor striatum is directly regulated by dopamine through D2 receptors located on corticostriatal terminals. By regulating a subset of terminals, dopamine release alters the parallel processing of cortical inputs to the striatum, affecting striatal excitation. Using dopamine-deficient mice and dopamine depleted mice, Bamford demonstrated that dopamine is not required during development for functional dopamine receptors. Dopamine depletion results in hypersensitive dopamine receptors that result in aberrant striatal function resulting in motor dyskinesias. Dopamine excess, as modeled by repeated use of amphetamine and methamphetamine, produces a chronic striatal depression that is renormalized by drug reinstatement. This effect is dose dependent, long lasting and is dependent on a new D1 receptor effect seen only in animals with previous psychostimulant experience. During withdrawal, a psychostimulant challenge produces a paradoxical increase in glutamate release. This increase in glutamate from depressed terminals appears to determine locomotor sensitization and the model extends to drug intake escalation both hallmarks of addiction. These findings received world-wide press coverage and included reports on BBC National and World Radio, ABC, Washington Post, Science and Nature, New Scientist, and Scientific American. Dr. Bamford also found that the huntingtin mutation produces age-dependent alterations in corticostriatal activity that is paralleled by a decrease in dopamine D2 receptor modulation of the presynaptic terminal. Taken together, these findings point to dynamic alterations in the corticostriatal pathway and emphasize that therapies directed toward alleviating or preventing symptoms need to be specifically designed depending on the progression of the disorder. This year, the Bamford lab showed how dopamine, endocannabinoids, and adenosine modulate frontal cortical projections to the nucleus accumbens (Wang et. Al., Journal of Physiology, 2012). In this study, we combined optical recordings of presynaptic release with whole-cell electrophysiology in CB1 receptor-null mice and bacterial artificial chromosome (BAC) transgenic mice to identify the specific interactions between dopamine and glutamate signaling at individual cortical terminals within the nucleus accumbens core. The work showed that 1) dopamine enhances cortical input to both D1- and D2 receptor-expressing medium spiny neurons (MSNs) in the nucleus accumbens core via presynaptic D1 receptors, suggesting a functional difference between dopamine-glutamate interactions in the ventral and dorsal striatum. 2) Dopamine specifically inhibits glutamate input to D2 receptor-expressing medium spiny neurons (MSNs) via D2 receptors in the absence of cortical activity and endocannabinoid signaling. 3) Dopamine indirectly inhibits presynaptic activity of both D1- and D2 receptor-expressing MSNs through adenosine, while endocannabinoids specifically-promote temporal- and activity-dependent filtering of cortical inputs to D2 receptor-bearing cells. 4) The direct excitatory actions by D1 receptors are occluded by striatal activation, which encourages adenosine release and corticoaccumbal inhibition. 5) The direct inhibitory actions by D2 receptors are occluded by striatal activation, which encourages endocannabinoid release and a broader inhibition of excitatory inputs. 6) Presynaptic inhibition by adenosine is dependent on AMPA and NMDA receptor activation as well as adenylate cyclase in D1R-bearing MSNs. Thus, the experiments showed that dopamine produces frequency-dependent filtering of low-probability release synapses. At low frequencies, D1 receptors excited striatal output neurons of the striatonigral pathway, while D2 receptors specifically inhibited neurons of the striatopallidal pathway. At higher frequencies, the dopamine-dependent release of adenosine and endocannabinoids promoted further temporal filtering of cortical signals entering both output pathways. These results help us understand how dopamine provides frequency and temporal filtering of cortical information by promoting activity through the striatonigral pathway, while inhibiting weak signals. Dr. Bamford also published a seminal article describing the behavioral effects of prenatal cocaine exposure (PCE) and the synaptic and biochemical mechanisms that might account for those behaviors. PCE remains a serious health problem and can produce significant developmental and motor disabilities in affected humans. Observations in the clinic and laboratory strongly suggest that PCE causes corticostriatal dysfunction, but this important pathway has never been investigated. In this manuscript, we used a murine model for PCE to characterize abnormal dopamine-dependent behaviors and synaptic plasticity of the corticostriatal pathway. Behavioral measures were combined with electrophysiology, optical imaging, biochemical and electrochemical recordings to identify the interactions between glutamate, GABA and dopamine signaling at individual cortical terminals within the motor striatum. We found that PCE reduces body growth and modifies dopamine-dependent motor behaviors in adolescent mice. Abnormal motor-learning and blunted locomotor responses to repeated amphetamine were paralleled by a reversible GABA-dependent over-inhibition at corticostriatal synapses and a reduction in phasic dopamine release capacity. The release of dopamine promoted normal corticostriatal filtering in controls, but alleviated GABA-mediated inhibition and paradoxically increased corticostriatal activity in those mice with a history of PCE. While GABAA receptors had no effect on presynaptic corticostriatal activity in controls, their inhibition normalized synaptic function following PCE and prevented D2 receptor-dependent paradoxical presynaptic potentiation suggesting new therapeutic avenues. In collaboration with the Palmiter laboratory, we showed that amphetamine sensitization requires balanced NMDA receptor activity in dopamine D1 and D2 receptor-expressing medium spiny neurons (Beutler et. al., PNAS, 2011) and that attenuating GABAA receptor signaling in dopamine neurons selectively enhances reward learning and alters risk preference in mice (Parker et. Al., J Neuroscience, 2011). In another paper published in Nature Neuroscience, we showed that the orphan G-protein-coupled receptor (GPCR) GPR88 is robustly expressed in medium spiny neurons in the striatum and regulated by neuro-pharmacological drugs. In the absence of GPR88, medium spiny neurons have increased glutamatergic excitation and reduced GABAergic inhibition that together promote enhanced firing rates in vivo, resulting in hyperactivity, poor motor-coordination, and impaired cue-based learning in mice. Targeted viral expression of GPR88 in medium spiny neurons rescues the molecular and electrophysiological properties and normalizes behavior, suggesting that aberrant MSN activation in the absence of GPR88 underlies behavioral deficits and its dysfunction may contribute to behaviors observed in neuropsychiatric disease (Quintana et. al., Nature Neuroscience, 2012). Further information can be obtained on the Bamford laboratory website http://depts.washington.edu/nigellab/index.html

Recommendations

  • Brea Nampa, ID 07.24.12

    Dr. Bamford is thorough and knowledgeable. Thanks to his careful diagnosis our sons have quality of life that they would not have otherwise had. We highly recommend him.

  • Julia Bellingham, Washington 04.26.12

    We found Dr. Bamford to be very thorough and thoughtful. I would recommend him highly.

Overview

Board Certification(s)

Neurology with Special Qualifications in Child Neu
Pediatrics

Medical/Professional School

University of Utah School of Medicine, Salt Lake City

Residency

Pediatrics, Columbia Presbyterian Hospital, New York
Child Neurology, Neurological Institute, New York

Clinical Interests

Movement disorders, cortical and cerebellar dysgenesis, toxicology, drug addiction and withdrawal

Research Description

The Bamford laboratory studies synaptic function and regulation of presynaptic activity. Presently, we are concentrating on the effects of dopamine on corticostriatal projections. In particular, we are interested in how dopamine depletion, Huntington's disease and psychostimulant withdrawal affect the release of glutamate from cortical projections to the striatum.

Lab URL

http://depts.washington.edu/nigellab/

Research Focus Area

Neuroscience / Neurodevelopment

Awards and Honors

Award Name Award Description Awarded By Award Date
Editorial Board, Pediatric Neurology Journal of Pediatric Neurology 2012
Nominated, Seattle Childrens Hospital Center Family Choice Award Seattle Childrens Hospital 2011
Nominated, Seattle Childrens Hospital Center Family Choice Award Seattle Childrens Hospital 2006
Nominated, Seattle Childrens Hospital Center Family Choice Award Seattle Childrens Hospital 2004
Young Investigator Award Child Neurology Society 2002
Teacher of the Year Award Department of Pediatrics, Lincoln Medical and Mental Health Center, Bronx, NY 2002
Nominated, Teacher of the Year Department of Pediatrics, Babies and Childrens Hospital, NY, NY 2001
Best of the Best Scientific Presentation, Scientific Highlights Plenary Session American Academy of Neurology 2000
Neurological Sciences Academic Development Award NIH 1997
First Place Resident Research Competition Tri-State Pediatric Neurology Society 1996
Senior Pediatric Honors Student University of Utah Medical School 1992
Drew B. Meilstrup Scholarship University of Utah Medical School 1991
Josephine Beam Scholarship for Outstanding Scholastic Achievement University of Utah 1988
Continuing Student Departmental Scholarship in Electrical Engineering University of Utah 1987
Junior College Transfer Scholarship University of Utah 1985 - 1987
ASUTC Award for Outstanding Scholastic Achievement (4.0 GPA) Salt Lake Community College 1985
Continuing Student Scholarship for Academic Excellence Salt Lake Community College 1984
Deans Departmental Scholarship in Electronic Technology Salt Lake Community College 1984
Merit Scholarship for Academic Excellence Salt Lake Community College 1983
Eagle Scout, Bronze Palm BSA 1977

Publications

  • Wang W, Darvas M, Storey GP, Bamford IJ, Gibbs JT, Palmiter RD, Bamford NS
    Acetylcholine encodes long-lasting presynaptic plasticity at glutamatergic synapses in the dorsal striatum after repeated amphetamine exposure.
    The Journal of neuroscience : the official journal of the Society for Neuroscience , 2013 June 19 : 33(25)10405-26
  • Wang W, Nitulescu I, Lewis JS, Lemos JC, Bamford IJ, Posielski NM, Storey GP, Phillips PE, Bamford NS
    Overinhibition of corticostriatal activity following prenatal cocaine exposure.
    Annals of neurology , 2013 Mar. : 73(3)355-69
  • Quintana A, Sanz E, Wang W, Storey GP, Güler AD, Wanat MJ, Roller BA, La Torre A, Amieux PS, McKnight GS, Bamford NS, Palmiter RD
    Lack of GPR88 enhances medium spiny neuron activity and alters motor- and cue-dependent behaviors.
    Nature neuroscience , 2012 Nov. : 15(11)1547-55
  • Quintana A, Sanz E, Wang W, Storey GP, Güler AD, Wanat MJ, Roller BA, La Torre A, Amieux PS, McKnight GS, Bamford NS, Palmiter RD
    Lack of GPR88 enhances medium spiny neuron activity and alters motor- and cue-dependent behaviors.
    Nature neuroscience , 2012 Nov. : 15(11)1547-55
  • Wang W, Nitulescu I, Lewis JS, Lemos JC, Bamford IJ, Posielski NM, Storey GP, Phillips PE, Bamford NS
    Overinhibition of corticostriatal activity following prenatal cocaine exposure.
    Annals of neurology , 2012 Nov.
  • Wang W, Dever D, Lowe J, Storey GP, Bhansali A, Eck EK, Nitulescu I, Weimer J, Bamford NS
    Regulation of prefrontal excitatory neurotransmission by dopamine in the nucleus accumbens core.
    The Journal of physiology , 2012 Aug. 15 : 590(Pt 16)3743-69
  • Wang W, Dever D, Lowe J, Storey GP, Bhansali A, Eck EK, Nitulescu I, Weimer J, Bamford NS
    Regulation of prefrontal excitatory neurotransmission by dopamine in the nucleus accumbens core.
    The Journal of physiology , 2012 Aug. : 590(Pt 16)3743-69
  • Nigel S. Bamford, MD
    Prospective Trial of a Pediatric Ventricular Assist Device
    New England Journal of Medicine , 2012 : 367532-41
  • Parker JG, Wanat MJ, Soden ME, Ahmad K, Zweifel LS, Bamford NS, Palmiter RD
    Attenuating GABA(A) receptor signaling in dopamine neurons selectively enhances reward learning and alters risk preference in mice.
    The Journal of neuroscience : the official journal of the Society for Neuroscience , 2011 Nov. 23 : 31(47)17103-12
  • Parker JG, Wanat MJ, Soden ME, Ahmad K, Zweifel LS, Bamford NS, Palmiter RD
    Attenuating GABA(A) receptor signaling in dopamine neurons selectively enhances reward learning and alters risk preference in mice.
    The Journal of neuroscience : the official journal of the Society for Neuroscience , 2011 Nov. : 31(47)17103-12
  • Beutler LR, Wanat MJ, Quintana A, Sanz E, Bamford NS, Zweifel LS, Palmiter RD
    Balanced NMDA receptor activity in dopamine D1 receptor (D1R)- and D2R-expressing medium spiny neurons is required for amphetamine sensitization.
    Proceedings of the National Academy of Sciences of the United States of America , 2011 Mar. 8 : 108(10)4206-11
  • Beutler LR, Wanat MJ, Quintana A, Sanz E, Bamford NS, Zweifel LS, Palmiter RD
    Balanced NMDA receptor activity in dopamine D1 receptor (D1R)- and D2R-expressing medium spiny neurons is required for amphetamine sensitization.
    Proceedings of the National Academy of Sciences of the United States of America , 2011 Mar. : 108(10)4206-11
  • Wong MY, Sulzer D, Bamford NS
    Imaging presynaptic exocytosis in corticostriatal slices.
    Methods in molecular biology (Clifton, N.J.) , 2011 : 793363-76
  • Wong MY, Sulzer D, Bamford NS
    Imaging presynaptic exocytosis in corticostriatal slices.
    Methods in molecular biology (Clifton, N.J.) , 2011 : 793363-76
  • Nigel S. Bamford, MD
    Alterations in Striatal Synaptic Function in Huntingtons and Parkinsons Diseases
    In: Handbook of Basal Ganglia Structure and Function, a Decade of Progress , 2010 : 607-623
  • Bamford NS, White KK, Robinett SA, Otto RK, Gospe SM Jr
    Neuromuscular hip dysplasia in Charcot-Marie-Tooth disease type 1A.
    Developmental medicine and child neurology , 2009 May : 51(5)408-11
  • Bamford NS, White KK, Robinett SA, Otto RK, Gospe SM Jr
    Neuromuscular hip dysplasia in Charcot-Marie-Tooth disease type 1A.
    Developmental medicine and child neurology , 2009 May : 408-11
  • Joshi PR, Wu NP, André VM, Cummings DM, Cepeda C, Joyce JA, Carroll JB, Leavitt BR, Hayden MR, Levine MS, Bamford NS
    Age-dependent alterations of corticostriatal activity in the YAC128 mouse model of Huntington disease.
    The Journal of neuroscience : the official journal of the Society for Neuroscience , 2009 Feb. 25 : 29(8)2414-27
  • Joshi PR, Wu NP, André VM, Cummings DM, Cepeda C, Joyce JA, Carroll JB, Leavitt BR, Hayden MR, Levine MS, Bamford NS
    Age-dependent alterations of corticostriatal activity in the YAC128 mouse model of Huntington disease.
    The Journal of neuroscience : the official journal of the Society for Neuroscience , 2009 Feb. : 29(8)2414-27
  • Nigel S. Bamford, MD
    The Corticostriatal Pathway in Parkinsons Disease
    In: Cortico-subcortical Dynamics in Parkinsons Disease , 2009 : 87-104
  • Bamford NS, Zhang H, Joyce JA, Scarlis CA, Hanan W, Wu NP, André VM, Cohen R, Cepeda C, Levine MS, Harleton E, Sulzer D
    Repeated exposure to methamphetamine causes long-lasting presynaptic corticostriatal depression that is renormalized with drug readministration.
    Neuron , 2008 Apr, 10 : 58(1)89-103
  • Bamford NS, Zhang H, Joyce JA, Scarlis CA, Hanan W, Wu NP, André VM, Cohen R, Cepeda C, Levine MS, Harleton E, Sulzer D
    Repeated exposure to methamphetamine causes long-lasting presynaptic corticostriatal depression that is renormalized with drug readministration.
    Neuron , 2008 Apr, : 89-103
  • Bamford NS, Robinson S, Palmiter RD, Joyce JA, Moore C, Meshul CK
    Dopamine modulates release from corticostriatal terminals.
    The Journal of neuroscience : the official journal of the Society for Neuroscience , 2004 Oct. 27 : 24(43)9541-52
  • Bamford NS, Robinson S, Palmiter RD, Joyce JA, Moore C, Meshul CK
    Dopamine modulates release from corticostriatal terminals.
    The Journal of neuroscience : the official journal of the Society for Neuroscience , 2004 Oct. : 9541-52
  • Bamford NS, Zhang H, Schmitz Y, Wu NP, Cepeda C, Levine MS, Schmauss C, Zakharenko SS, Zablow L, Sulzer D
    Heterosynaptic dopamine neurotransmission selects sets of corticostriatal terminals.
    Neuron , 2004 May 27 : 42(4)653-63
  • Bamford NS, Zhang H, Schmitz Y, Wu NP, Cepeda C, Levine MS, Schmauss C, Zakharenko SS, Zablow L, Sulzer D
    Heterosynaptic dopamine neurotransmission selects sets of corticostriatal terminals.
    Neuron , 2004 May : 653-63
  • Bamford NS, Trojaborg W, Sherbany AA, De Vivo DC
    Congenital Guillain-Barré syndrome associated with maternal inflammatory bowel disease is responsive to intravenous immunoglobulin.
    European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society , 2002 : 6(2)115-9
  • Bamford NS, Trojaborg W, Sherbany AA, De Vivo DC
    Congenital Guillain-Barr syndrome associated with maternal inflammatory bowel disease is responsive to intravenous immunoglobulin.
    European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society , 2002 : 115-9
  • Nigel S. Bamford, MD
    Varicella-Zoster Virus Retrobulbar Optic Neuritis in a Patient with Human Immunodeficiency Virus
    Am J Ophthal , 1996 : 122(4)586-588

Presentations

Presentations Title Event Location Date
Targeting GABA-A receptors for treatment of behaviors following prenatal cocaine exposure Child Neurology Society Annual Meeting Austin, TX Oct. 2013
GABA Interneurons and Prenatal Cocaine; a little goes a long way Grand Rounds, Neurological Institute Coumbia Univarsity Feb. 2013
Repeated Amphetamine Causes Long-Lasting Plasticity at Corticostriatal Synapses Winter Conference on Brain Research Snowbird, UT Jan. 2012
Lasting impressions of novel experience are encoded in basal ganglia circuits Child Neurology Society Annual Meeting Savannah GA Oct. 2011
Neurology Grand Rounds Stanford University Neuronal circuitry for attention, movements and very bad habits March 2011
Prenatal cocaine exposure causes a GABA-dependent reversal in D2 dopamine receptor responses at corticostriatal synapses Winter Conference on Brain Research Keystone, CO Jan. 2011
Gestational cocaine exposure causes a GABAA-mediated reversal in D2 dopamine receptor responses at corticostriatal synapses Child Neurology Society Annual Meeting Providence, RI Oct. 2010
D2 and D5 dopamine receptors in the dorsal striatum contribute to habit learning and substance abuse Child Neurology Society Annual Meeting Providence, RI Oct. 2010
Behaviors are regulated by long-term synapse plasticity within the nucleus accumbens core Child Neurology Society Annual Meeting Providence, RI Oct. 2010
Effects of D2 dopamine receptors on corticostriatal synapses The Lieber Center for Schizophrenia Research and Treatment. Seminar Series Columbia University Oct. 2010
Gestational cocaine exposure causes reversible plasticity at corticostriatal synapses Research Seminar University of Chicago July 2010
Anatomical and Functional Variations in Striatal Synaptic Control Child Neurology Society Annual Meeting Louisville, TN Oct. 2009
Huntington Mutation Produces Age-Dependent Alterations in Striatal Excitation in YAC128 transgenic mice Child Neurology Society Annual Meeting Santa Clara, CA Oct. 2008
Biphasic changes of corticostriatal activity in the YAC128 mouse model of Huntingtons disease 12th International Conference on In Vivo Methods Vancouver, BC Aug. 2008
Methamphetamine Addiction Mechanism is Identified BBC Radio World Service. Science in Action with John Stewart April 11, 2008
The Brain Circuitry in Drug Addiction BBC Radio 4. Leading Edge with Geoff Watts April 10, 2008
Regulation of Glutamate Release in the Ventral Striatum Winter Conference on Brain Research Jan. 2008
Glutamate Release in the Ventral Striatum is Mediated by D1 and D2 Receptor Activity Child Neurology Society Annual Meeting Qubec City, Canada Oct. 2007
Methamphetamine Induces Locomotor Changes and Striatal Synaptic Plasticity that are Dependent on D1 Dopamine-Receptors Child Neurology Society Annual Meeting Qubec City, Canada Oct. 2007
Synaptic Mechanisms in Motor Learning North Pacific Pediatric Neurology Colloquium Seattle, WA June 2007
Dopamine Function in Models of Neurological and Psychiatric Disorders Winter Conference on Brain Research Steamboat Springs, CO Jan. 2006
Chronic Methamphetamine Mediates Long-Term Depression of Corticostriatal Release in the Dorsal Striatum Child Neurology Society Annual Meeting Los Angeles, CA Aug. 2005
Presynaptic Regulation of Corticostriatal Terminals by Acetylcholine Unveiled During Amphetamine Withdrawal Gordon Research Conference Proctor Academy, NH July 2005
Synaptic Plasticity in Neonatal Psychostimulant Withdrawal Pacific Northwest and Western Canada Pediatric Neurology Colloquium Vancouver BC May 2005
Receptor Hypersensitivity in Dopamine Depletion North Pacific Pediatric Neurology Colloquium Seattle, WA May 2004
Psychostimulants Depress Cortical Excitation of the Striatum, an Effect Mediated by Presynaptic Corticostriatal D2 Dopamine Receptors Child Neurology Society Annual Meeting Miami FL Oct. 2003
Corticostriatal Signaling in Huntingtons Disease Mutant Mice Mental Retardation Research Center Research Seminar UCLA, CA July 2003
Presynaptic Activity of Corticostriatal Terminals is Regulated by D2 Dopamine Receptors Child Neurology Society Young Investigator Award Lecture Washington DC Oct. 2002
Defects in Cell Migration in Zellweger Syndrome Pediatric Grand Round Lincoln Medical and Mental Health Center, Bronx, NY March 2001
Neuronal Migration and Apoptosis in the Newborn Zellweger Transgenic Mouse American Academy of Neurology May 2000

Research Funding

Grant Title Grantor Amount Award Date
Psychostimulant-induced changes in striatal cholinergic interneuron physiology University of Washington Alcohol and Drug Abuse Institute $ 2012 - 2014
Dopamine-Induced Striatal Synaptic Plasticity NIH 2009 - 2010
Training in Molecular Pharmacology of Abused Drugs NIH $ 2009 - 2014
Berlin Heart EXCOR Pediatric Ventricular Assist Device Seattle Childrens Hospital 2008 - 2009
Gestational Cocaine Exposure Mediates Long-Term Changes in Striatal Function University of Washington Alcohol and Drug Abuse Institute 2007 - 2009
Dopamine-Induced Striatal Synaptic Plastici NIH $ 2007 - 2014
Excitotoxic glutamatergic corticostriatal projections mediate striatal damage in Huntington's mutant mice UW Royalty Research Fund 2003 - 2004
Presynaptic activity of corticostriatal terminals is regulated by D2 dopamine receptors Child Neurology Society Young Investigator Award 2002 - 2008
Neurological Sciences Academic Development Award NIH 1997 - 2002