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Khaled Moussawi, M.D., Ph.D.

Khaled Moussawi, M.D., Ph.D.

Position

Former Special Volunteer, Office of the Clinical Director

Contact

Biomedical Research Center
251 Bayview Boulevard
Suite 200
Baltimore, MD 21224

Email: khaled.moussawi@nih.gov

Education

M.D./Ph.D. Medical University of South Carolina

Research Interests

Dr. Khaled Moussawi completed his undergraduate degree in Biology at the American University of Beirut in Lebanon before joining the MD/PhD program at the Medical University of South Carolina for his medical and doctoral training. He then finished his neurology residency at the Partners Neurology program, affiliated with Massachusetts General Hospital, Brigham and Women’s Hospital and Harvard Medical School. In 2016, Khaled completed a clinical fellowship in Neuropsychiatry at Johns Hopkins. He is currently a clinical fellow at NIDA and an Adjunct Faculty in the Neurology department at Hopkins. His research interests involve using neuromodulation to treat neuropsychiatric disorders such as drug addiction.

Selected Publications

2018

Francis, Tanner Chase; Gantz, Stephanie C; Moussawi, Khaled; Bonci, Antonello

Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine. Journal Article

In: Curr Opin Neurobiol, vol. 54, pp. 66–72, 2018, ISSN: 1873-6882 (Electronic); 0959-4388 (Linking).

Abstract | Links

@article{Francis:2018aa,
title = {Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine.},
author = {Tanner Chase Francis and Stephanie C Gantz and Khaled Moussawi and Antonello Bonci},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30237117},
doi = {10.1016/j.conb.2018.08.013},
issn = {1873-6882 (Electronic); 0959-4388 (Linking)},
year = {2018},
date = {2018-09-17},
journal = {Curr Opin Neurobiol},
volume = {54},
pages = {66--72},
address = {Intramural Research Program, Synaptic Plasticity Section, National Institute on Drug Abuse, US National Institutes of Health, Baltimore, MD 21224, USA.},
abstract = {Cocaine exposure induces persistent changes in synaptic transmission and intrinsic properties of ventral tegmental area (VTA) dopamine neurons. Despite significant progress in understanding cocaine-induced plasticity, an effective treatment of cocaine addiction is lacking. Chronic cocaine potentiates excitatory and alters inhibitory transmission to dopamine neurons, induces dopamine neuron hyperexcitability, and reduces dopamine release in projection areas. Understanding how intrinsic and synaptic plasticity interact to control dopamine neuron firing and dopamine release could prove useful in the development of new therapeutics. In this review, we examine recent literature discussing cocaine-induced plasticity in the VTA and highlight potential therapeutic interventions.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}

Close

Cocaine exposure induces persistent changes in synaptic transmission and intrinsic properties of ventral tegmental area (VTA) dopamine neurons. Despite significant progress in understanding cocaine-induced plasticity, an effective treatment of cocaine addiction is lacking. Chronic cocaine potentiates excitatory and alters inhibitory transmission to dopamine neurons, induces dopamine neuron hyperexcitability, and reduces dopamine release in projection areas. Understanding how intrinsic and synaptic plasticity interact to control dopamine neuron firing and dopamine release could prove useful in the development of new therapeutics. In this review, we examine recent literature discussing cocaine-induced plasticity in the VTA and highlight potential therapeutic interventions.

Close

  • https://www.ncbi.nlm.nih.gov/pubmed/30237117
  • doi:10.1016/j.conb.2018.08.013

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  • Contact Us
  • Careers at NIDA IRP
  • Accessibility
  • Privacy
  • HHS Vulnerability Disclosure
  • Freedom of Information Act
  • Document Viewing Tools
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    • Cellular and Neurocomputational Systems Branch
    • Molecular Neuropsychiatry Research Branch
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