Ph.D. Brown University, 1996
Sc.M. Brown University, 1993
B.Sc. Brown University, 1988
Email address: hohmanna(at)indiana.edu
My research has focused on understanding pain modulation from a neurochemical perspective. The discovery of cannabinoid receptors and identification of brain constituents that act at these receptors established the existence of an endogenous cannabis-like (endocannabinoid) transmitter system. My research has identified functional roles of the endocannabinoid system in the nervous system and mapped it's distribution in sensory pathways. My research has identified enzymes implicated in endocannabinoid deactivation as novel therapeutic targets. My laboratory strives to maximize the therapeutic potential of endocannabinoid signaling systems while minimizing unwanted central nervous system side-effects (e.g. psychoactivity and addiction). My research program combines behavioral, drug self-administration, neuroanatomical, neurophysiological and molecular approaches to study cannabinoid mechanisms for suppression of pain and stress responsiveness.
Please search for "A. G. Hohmann" on PubMed to view recent publications from this investigator.
Guindon J, Lai Y, Takacs SM, Bradshaw HB, Hohmann AG. (2013). Alterations in endocannabinoid tone following chemotherapy-induced peripheral neuropathy: effects of endocannabinoid deactivation inhibitors targeting fatty-acid amide hydrolase and monoacylglycerol lipase in comparison to reference analgesics following cisplatin treatment. Pharmacol. Res., 67, 94-109.
Guindon J, Hohmann AG. (2013). Use of sodium bicarbonate to promote weight gain, maintain body temperature, normalize renal functions and minimize mortality in rodents receiving the chemotherapeutic agent cisplatin. Neurosci. Lett., 544, 41-46.
Deng L, Guindon J, Vemuri VK, Thakur GA, White FA, Makriyannis A, Hohmann AG. (2012). The maintenance of cisplatin- and paclitaxel-induced mechanical and cold allodynia is suppressed by cannabinoid CB(2) receptor activation and independent of CXCR4 signaling in models of chemotherapy-induced peripheral neuropathy. Mol. Pain, 8, 71.
Gregg LC, Jung KM, Spradley JM, Nyilas R, Suplita RL, 2nd, Zimmer A, Watanabe M, Mackie K, Katona I, Piomelli D, Hohmann AG. (2012). Activation of type 5 metabotropic glutamate receptors and diacylglycerol lipase-alpha initiates 2-arachidonoylglycerol formation and endocannabinoid-mediated analgesia. J. Neurosci., 32, 9457-9468.
Sciolino NR, Zhou W, Hohmann AG. (2011). Enhancement of endocannabinoid signaling with JZL184, an inhibitor of the 2-arachidonoylglycerol hydrolyzing enzyme monoacylglycerol lipase, produces anxiolytic effects under conditions of high environmental aversiveness in rats. Pharmacol. Res., 64, 226-234.
Rahn EJ, Thakur GA, Wood JA, Zvonok AM, Makriyannis A, Hohmann AG. (2011). Pharmacological characterization of AM1710, a putative cannabinoid CB2 agonist from the cannabilactone class: antinociception without central nervous system side-effects. Pharmacol. Biochem. Behav., 98, 493-502.
Clapper JR, Moreno-Sanz G, Russo R, Guijarro A, Vacondio F, Duranti A, Tontini A, Sanchini S, Sciolino NR, Spradley JM, Hohmann AG, Calignano A, Mor M, Tarzia G, Piomelli D. (2010). Anandamide suppresses pain initiation through a peripheral endocannabinoid mechanism. Nat. Neurosci., 13, 1265-1270.
Sciolino NR, Bortolato M, Eisenstein SA, Fu J, Oveisi F, Hohmann AG, Piomelli D. (2010). Social isolation and chronic handling alter endocannabinoid signaling and behavioral reactivity to context in adult rats. Neuroscience, 168, 371-386.
Spradley JM, Guindon J, Hohmann AG. (2010). Inhibitors of monoacylglycerol lipase, fatty-acid amide hydrolase and endocannabinoid transport differentially suppress capsaicin-induced behavioral sensitization through peripheral endocannabinoid mechanisms. Pharmacol. Res., 62, 249-258.