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Aron H. Lichtman, Ph.D. Aron H. Lichtman, Ph.D.
Professor
1220 East Broad St.
Molecular Medicine Research Building Room 3042
P.O. Box 980613
Richmond, Virginia 23298-0613
Phone: (804) 828-8480
E-mail: alichtma@vcu.edu
Publications: selected | PubMed
Personal web
 

Education: Dartmouth College, 1989

Research interests:  Cannabinoids; drugs of abuse; learning and memory; pain and inflammation

My research program focuses on four general areas: 1) understanding the physiological function of the endocannabinoid system; 2) elucidating the mechanisms of action underlying the pharmacological effects of THC and other cannabinoids; 3) investigating medicinal uses of cannabinoids and 4) determining the impact of the drugs of abuse via the inhalation route of administration. Much of this research employs a multidisciplinary approach using a combination of behavioral/physiological measures, pharmacological agents, genetically altered mice, and quantification of drug as well as endogenous compounds in body and brain. The endocannabinoid system in the central nervous system is comprised of the endogenous cannabinoids arachidonoylethanolamide (anandamide) and the monoacylglycerol 2-arachidonoylglycerol (2-AG) that bind to CB1 cannabinoid receptors in the brain and spinal cord. Most recently we have found that the enzyme fatty acid amide hydrolase (FAAH) is a key in vivo regulator of anandamide and other fatty acid amides, which sets an endogenous tone that modulates several physiological functions including the modulation of pain, inflammation, cognition, and drug dependence. In addition, we have found that disruption of endocannabinoid signaling facilitates the extinction of non-reinforced behavior from memory. These extinction deficits appear in some models as improved memory; while in tasks that require the suppression of previously learned responses they appear as a disruption in learning. Finally, other research in my laboratory demonstrates the FAAH modulates both pain and inflammatory responses. This work taken together may ultimately contribute to the development of endocannabinoid/FAAH-based therapeutic agents for the treatment of pain, cognitive disorders and drug addiction. .

Selected publications:

Schlosburg JE, O'Neal ST, Conrad DH, and Lichtman AH. (2011) CB(1) receptors mediate rimonabant-induced pruritic responses in mice: investigation of locus of action. Psychopharmacology (Berl).  [Epub ahead of print]

Soderstrom K, Poklis JL, and Lichtman AH. (2011) Cannabinoid exposure during zebra finch sensorimotor vocal learning persistently alters expression of endocannabinoid signaling elements and acute agonist responsiveness. BMC Neurosci. 12:3.

Kinsey SG, O'Neal ST, Long JZ, Cravatt BF, and Lichtman AH. (2011) Inhibition of endocannabinoid catabolic enzymes elicits anxiolytic-like effects in the marble burying assay. Pharmacol Biochem Behav. 98(1):21-7.

Kinsey SG, Mahadevan A, Zhao B, Sun H, Naidu PS, Razdan RK, Selley DE, Imad Damaj M, and Lichtman AH. (2011) The CB(2) cannabinoid receptor-selective agonist O-3223 reduces pain and inflammation without apparent cannabinoid behavioral effects. Neuropharmacology. 60(2-3):244-51.

Poklis JL, Thompson CC, Long KA, Lichtman AH, and Poklis A. (2010) Disposition of Cannabichromene, Cannabidiol, and Δ-Tetrahydrocannabinol and its Metabolites in Mouse Brain following Marijuana Inhalation Determined by High-Performance Liquid Chromatography-Tandem Mass Spectrometry. J Anal Toxicol. 34(8):516-520.

Bu DX, and Lichtman AH. (2010) T cells and blood vessels: costimulation turns up the pressure. Circulation. 122(24):2495-8.

Avraham Y, Saidian M, Burston JJ, Mevorach R, Vorobiev L, Magen I, Kunkes E, Borges B, Lichtman AH, and Berry EM. (2010) Fish oil promotes survival and protects against cognitive decline in severely undernourished mice by normalizing satiety signals. J Nutr Biochem. [Epub ahead of print]

Lichtman AH, Blankman JL, and Cravatt BF. (2010) Endocannabinoid overload. Mol Pharmacol. 78(6):993-5.

Schlosburg JE, Blankman JL, Long JZ, Nomura DK, Pan B, Kinsey SG, Nguyen PT, Ramesh D, Booker L, Burston JJ, Thomas EA, Selley DE, Sim-Selley LJ, Liu QS, Lichtman AH, and Cravatt BF. (2010) Chronic monoacylglycerol lipase blockade causes functional antagonism of the endocannabinoid system. Nat Neurosci. 13(9):1113-9.

DeLong GT, Wolf CE, Poklis A, and Lichtman AH. (2010) Pharmacological evaluation of the natural constituent of Cannabis sativa, cannabichromene and its modulation by Δ(9)-tetrahydrocannabinol. Drug Alcohol Depend. 2010 Nov 1;112(1-2):126-33.

Kinsey SG, Long JZ, Cravatt BF, and Lichtman AH. (2010) Fatty acid amide hydrolase and monoacylglycerol lipase inhibitors produce anti-allodynic effects in mice through distinct cannabinoid receptor mechanisms. J Pain. 11(12):1420-8.

Bu DX, Tarrio M, Grabie N, Zhang Y, Yamazaki H, Stavrakis G, Maganto-Garcia E, Pepper-Cunningham Z, Jarolim P, Aikawa M, García-Cardeña G, and Lichtman AH. (2010) Statin-induced Krüppel-like factor 2 expression in human and mouse T cells reduces inflammatory and pathogenic responses. J Clin Invest. 2010 Jun 1;120(6):1961-70.

Naidu PS, Kinsey SG, Guo TL, Cravatt BF, and Lichtman AH. (2010) Regulation of inflammatory pain by inhibition of fatty acid amide hydrolase. J Pharmacol Exp Ther. 334(1):182-90.

Falenski KW, Thorpe AJ, Schlosburg JE, Cravatt BF, Abdullah RA, Smith TH, Selley DE, Lichtman AH, and Sim-Selley LJ. (2010) FAAH-/- mice display differential tolerance, dependence, and cannabinoid receptor adaptation after delta 9-tetrahydrocannabinol and anandamide administration. Neuropsychopharmacology. 35(8):1775-87.

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