Program Director/Principal Investigator (Last, First, Middle):
Kirken, Robert A.
BIOGRAPHICAL SKETCH
Provide the following information for the Senior/key personnel and other significant contributors in the order listed on Form Page 2.
Follow this format for each person. DO NOT EXCEED FOUR PAGES.
NAME
POSITION TITLE
Arshad Mahmood Khan
Assistant Professor
eRA COMMONS USER NAME (credential, e.g., agency login)
arshadk
EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, include postdoctoral training and
residency training if applicable.)
DEGREE
INSTITUTION AND LOCATION
MM/YY
FIELD OF STUDY
(if applicable)
University of California, Riverside, CA
B.S.
06/94
Biology/Biochemistry
(double major)
University of California, Riverside, CA
University of California, Riverside, CA
Univ. of Southern California, Los Angeles, CA
Univ. of Southern California, Los Angeles, CA
M.S.
Ph.D.
12/96
03/02
2002-2004
2004-2007
Biochemistry
Neuroscience
Postdoctoral associate
Postdoc. fellow (NRSA)
A. Personal Statement
The research goal of my laboratory within the Border Biomedical Research Center is to identify the neural
substrates underlying feeding stimulation, body weight regulation and glucosensing, with an aim to identify
novel targets for drug treatments against diabetes, obesity and other metabolic disorders disproportionately
affecting individuals in the Paso del Norte region along the U.S.-Mexico border. I focus using rodent models to
identify a subset of neural circuits related to feeding control that are distributed in the hypothalamus, and how
these circuits make connections with regions controlling the rewarding and reinforcing aspects of food. We
especially focus on the interactions between small neurotransmitters (glutamate) and neuropeptides
(neuropeptide Y, Agouti gene related peptide, hypocretin/orexin, melanin-concentrating hormone) in mediating
prolonged feeding stimulation. Additionally, we are interested in how these orexigenic signals may be impaired
in conditions such as obesity, diabetes and hypoglycemia-associated autonomic failure. Such impairments
may increase the vulnerability individuals with metabolic syndrome may have to other illnesses. A basic
understanding of these impairments is critical for developing rational therapeutics targeting feeding- and
metabolic-control circuits in the brain.
B. Positions, Honors and Affiliations
1. Employment
1994-2002
Grad Student (MS/PhD), Dept. of Cell Biology & Neuroscience, UC Riverside
2002-2004
Postdoctoral Associate, Biology Dept, University of Southern California
2004-2007
Postdoctoral Fellow, Biology Dept, University of Southern California
2007-2010
Research Assistant Professor, Biology Dept, University of Southern California
2011-
Adjunct Assistant Professor, Biology Dept, University of Southern California
Jan 2011-
Assistant Professor (tenure track), Biology Dept, Univ of Texas at El Paso
2. Honors
1995
Election to Sigma Xi, Scientific Honor Society
1995
James & Margaret Lesley Prize for Completed Original Research
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Program Director/Principal Investigator (Last, First, Middle):
Kirken, Robert A.
1998
Frances Marlatt Baugh Award for Outstanding Graduate Research
2000
Graduate Division Dean’s Dissertation Research Grant
2004
NIH Postdoctoral Fellowship: “Signal Transduction Mechanisms in
Neuroendocrine Neurons” 4.3 percentile rank
2004
Co-recipient, eSciences Funding Award from Microsoft Research; Title:
“Sangam: A System for Integrating Data to Solve Stress-Circuitry-Gene
Coupling”; one of five applications awarded from a pool of nearly 400 proposals.
2008
NIH Mentored Career Development Award (K01); Title: “From Glucosensing
Neurons to CRH Neuroendocrine Neurons: Circuits and Signals”
2010
Travel Award, Winter Conference on Brain Research
3. Membership in Professional Societies
Society for Neuroscience, International Society for Neurochemistry, International Society for the History of
the Neurosciences
C. Selected Peer-Reviewed Publications (in chronological order)
1. Gillard ER, Khan AM, Haq AU, Grewal RS, Mouradi B, Stanley BG. (1997) Stimulation of eating by the
second messenger cAMP in the perifornical and lateral hypothalamus. American Journal of Physiology
273:R107-R112.
2. Stanley BG, Gillard ER, Khan AM. (1998) Physiological Controls of Eating and Body Weight. In:
Encyclopedia of Mental Health, Vol. 2 (H.S. Friedman, ed.-in-chief), pp. 59-75; San Diego: Academic
Press.
3. Gillard ER, Khan AM, Mouradi B, Nalamwar O, Stanley BG. (1998) Eating induced by perifornical
cAMP is behaviorally selective and involves protein kinase activity. American Journal of Physiology,
275:R647-R653.
4. Miyata S, Khan AM, Hatton GI. (1998) Colocalization of calretinin and calbindin-D28k with oxytocin and
vasopressin in rat supraoptic nucleus neurons: A quantitative study. Brain Research, 785:178-182.
5. Gillard ER, Khan AM, Grewal RS, Mouradi B, Wolfsohn SD, Stanley BG. (1998) The second
messenger cyclic AMP elicits eating by an anatomically specific action in the perifornical hypothalamus.
The Journal of Neuroscience, 18:2646-2652.
6. Khan AM, Currás MC, Jamal FA, Turkowski CA, Goel RK, Dao J, Gillard ER, Wolfsohn SD, Stanley
BG. (1999) Lateral hypothalamic NMDA receptor subunits NR2A and/or NR2B mediate eating:
Immunochemical/behavioral evidence. American Journal of Physiology, 276:R880-R891.
7. Burns GAPC, Khan AM, Ghandeharizadeh S, O’Neill MA, Chen Y-S. (2003) Practical tools and
approaches for the construction of knowledge models from the neuroscientific literature.
Neuroinformatics, 1:81-109.
8. Khan AM, Watts AG. (2004) Intravenous 2-deoxy-D-glucose injection rapidly elevates levels of the
phosphorylated forms of p44/42 mitogen activated protein kinases (ERK1/2) in rat hypothalamic
parvicellular paraventricular neurons. Endocrinology, 145(1):351-359.
9. Khan AM, Cheung HH, Gillard ER, Palarca JA, Welsbie DS, Gurd JW, Stanley BG. (2004) Lateral
hypothalamic signaling mechanisms underlying feeding stimulation: Differential contributions of Src
family tyrosine kinases to feeding triggered either by NMDA injection or by food deprivation. The
Journal of Neuroscience, 24:10603-10615.
10. Khan AM, Hahn J, Cheng W-C, Watts AG, Burns GAPC. (2006) NeuroScholar’s electronic laboratory
notebook and its application to neuroendocrinology. Neuroinformatics, 4(2):139-160.
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Program Director/Principal Investigator (Last, First, Middle):
Kirken, Robert A.
11. Watts AG, Khan AM, Sanchez-Watts G, Salter D, Neuner CM. (2006) Activation in neural networks
controlling ingestive behaviors: What does it mean and how do we map and measure it? Physiology
and Behavior, 89(4):501-510.
12. Gorton LM, Khan AM, Bohland MA, Sanchez-Watts G, Donovan CM, Watts AG. (2007) A major role for
the forebrain in mediating time-of-day differences in glucocorticoid counterregulatory responses to
hypoglycemia. Endocrinology, 148(12):6026-6039.
13. Khan AM, Ponzio TA, Sanchez-Watts G, Stanley BG, Hatton GI, Watts AG. (2007) Catecholaminergic
control of MAP kinase signaling in paraventricular neuroendocrine neurons in vivo and in vitro: A
proposed role during glycemic challenges. The Journal of Neuroscience, 27(27):7344-7360. [Article
featured in the journal’s “This Week in the Journal” section].
14. Khan AM. (2009). Nerve, muscle, blood, toil, tears, and sweat: England’s pioneering biophysicist,
soldier, and statesman. Journal of the History of the Neurosciences, 18(1):80-81; 98-105.
15. Khan AM, Kaminski KL, Sanchez-Watts G, Ponzio TA, Kuzmiski JB, Bains JS, Watts AG. (2011). MAP
kinases couple hindbrain-derived catecholamine signals to hypothalamic adrenocortical control
mechanisms during glycemia-related challenges. The Journal of Neuroscience, 31(50):18479-18491.
D. Current Research Support
Ongoing Research Support:
K01DK01897 (Arshad Khan, PI) 09/10/2008- 07/31/2013
NIH/NIDDK
From Glucosensing Neurons to CRH Neuroendocrine Neurons: Circuits and Signals
The proposed research focuses on defining the chemical phenotypes of glucosensing neurons in the brain
that respond to glycemic challenges and to define the circuits between these regions and the
paraventricular hypothalamus, which helps the organism respond to these challenges by initiating
glucocorticoid responses. Additionally, the plan also focuses on the regulation of PVH neurons by signals
that are released by these glucosensing regions.
8G12MD007592-19 (Arshad Khan, PI; Manuel Llano, Co-PI) 07/01/2012-06/30/2013
NCRR/NIMHD (NIH)
BBRC Pilot Grant:
Optogenetic study of hypocretin neurons in glucosensing and hypoglycemia unawareness
This project addresses a serious complication of diabetes, known as hypoglycemia associated autonomic
failure (HAAF), which is known to affect patients frequently and for which basic understanding is currently
lacking. The project links two separate BBRC research units — Neuroscience and Metabolic Disorders (PI:
Khan) and Infectious Disease (Co-PI: Llano) — to address a significant border health issue. The goal of
this project is to rescue the autonomic responses in a rat model of HAAF by optical stimulation of neurons
in the lateral hypothalamus.
5G12RR008124/8G12MD007592 (Diana Natalicio, PI); 1998-2014
NCRR/NIMHD (NIH)
Border Biomedical Research Center
University of Texas at El Paso
Start-up funds for new investigators
0925-0001/0002 (Rev. 08/12)
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