Indiana University
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The Gill Center for Biomolecular Science

Andrea G. Hohmann | Faculty

Andrea G. HohmannProfessor, Department of Psychological and Brain Sciences and Program in Neuroscience

Office: MSBII 220
TEL: 812-856-0672
Email: hohmanna@indiana.edu

Lab Website

Education

  • Brown University, Ph.D., 1996
  • Brown University, Sc.M., 1993
  • Brown University, Sc.B., 1988

Research Interests

  • Neuroscience
  • Biology & behavior

Functional roles of the brain's own cannabis-like (endocannabinoid) system in the nervous system; mechanisms of pain and analgesia; mechanisms of action of drugs of abuse; novel therapeutics

Research Statement

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.

Representative Publications

  • Please search for "A. G. Hohmann" on PubMed to view recent publications from this investigator.
  • Crystal JD, Alford WT, Zhou W, Hohmann A.G. Source memory in the rat. Curr Biol. 2013;23:387-91.
  • Guindon J, Lai Y, Takacs SM, Bradshaw HB, Hohmann A.G. 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. 2013;67:94-109.
  • Guindon J, Hohmann A.G. 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. 2013.
  • Deng L, Guindon J, Vemuri VK, Thakur GA, White FA, Makriyannis A, Hohmann A.G. 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. 2012;8:71.
  • Gregg LC, Jung KM, Spradley JM, Nyilas R, Suplita RL, 2nd, Zimmer A, Watanabe M, Mackie K, Katona I, Piomelli D, Hohmann A.G. Activation of type 5 metabotropic glutamate receptors and diacylglycerol lipase-alpha initiates 2-arachidonoylglycerol formation and endocannabinoid-mediated analgesia. J Neurosci. 2012;32:9457-68.
  • Zhou W, Hohmann A.G, Crystal JD. Rats answer an unexpected question after incidental encoding. Curr Biol. 2012;22:1149-53.
  • Guindon J, Hohmann A.G. The endocannabinoid system and cancer: therapeutic implication. Br J Pharmacol. 2011;163:1447-63.
  • Gutierrez T, Crystal JD, Zvonok AM, Makriyannis A, Hohmann A.G. Self-medication of a cannabinoid CB2 agonist in an animal model of neuropathic pain. Pain. 2011;152:1976-87.
  • Sciolino NR, Zhou W, Hohmann A.G. 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. 2011;64:226-34.
  • Guindon J, Guijarro A, Piomelli D, Hohmann A.G. Peripheral antinociceptive effects of inhibitors of monoacylglycerol lipase in a rat model of inflammatory pain. Br J Pharmacol. 2011;163:1464-78.
  • Rahn EJ, Thakur GA, Wood JA, Zvonok AM, Makriyannis A, Hohmann A.G. Pharmacological characterization of AM1710, a putative cannabinoid CB2 agonist from the cannabilactone class: antinociception without central nervous system side-effects. Pharmacol Biochem Behav. 2011;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 A.G, Calignano A, Mor M, Tarzia G, Piomelli D. Anandamide suppresses pain initiation through a peripheral endocannabinoid mechanism. Nat Neurosci. 2010;13:1265-70.
  • Sciolino NR, Bortolato M, Eisenstein SA, Fu J, Oveisi F, Hohmann A.G, Piomelli D. Social isolation and chronic handling alter endocannabinoid signaling and behavioral reactivity to context in adult rats. Neuroscience. 2010;168:371-86.
  • Spradley JM, Guindon J, Hohmann A.G. Inhibitors of monoacylglycerol lipase, fatty-acid amide hydrolase and endocannabinoid transport differentially suppress capsaicin-induced behavioral sensitization through peripheral endocannabinoid mechanisms. Pharmacol Res. 2010;62:249-58.
  • Eisenstein, S.A., Clapper, J., Holmes, P.V., Piomelli, D. and Hohmann, A.G. (2010) A role for 2-arachidonoylglycerol and endocannabinoid signaling in the locomotor response to novelty induced by olfactory bulbectomy. Pharmacological Research 61: 419-429.
  • Guindon, J. and Hohmann, A.G. (2009) The endocannabinoid system and pain. CNS & Neurological Disorders-Drug Target 8 (6) 403-421.
  • Rahn, E.J. and Hohmann, A.G. (2009) Cannabinoids as pharmacotherapies for neuropathic pain: from the bench to the bedside. Neurotherapeutics 6: 713-737.
  • Rahn, E.J., Zvonok, A.M., Thakur, G., Khanolkar, A.D. Makriyannis, A. and Hohmann, A.G. (2008) Selective activation of cannabinoid CB2 receptors suppresses neuropathic nociception evoked by the chemotherapeutic agent paclitaxel in rats. Journal of Pharmacology and Experimental Therapeutics 327: 584-591.
  • Moise, A.M., Eisenstein, S.A., Astarita, G., Piomelli, D. and Hohmann, A.G. (2008) An endocannabinoid signaling system modulates anxiety-like behavior in male Syrian hamsters. Psychopharmacology 200: 333-346.
  • Suplita II, R.L., Farthing, J., Gutierrez, T. and Hohmann, A.G. (2005) Inhibition of fatty-acid amide hydrolase enhances cannabinoid stress-induced analgesia: Sites-of-action in the dorsolateral periaqueductal gray and rostral ventromedial medulla. Neuropharmacology 49:1201-1209.
  • Hohmann, A.G., Suplita II, R.L., Bolton, N.M., Neely, M.H., Fegley, D., Mangieri, R., Krey, J.F., Walker, J.M., Holmes, P.V., Crystal, J.D., Duranti, A., Tontini, M., Tarzia G. and Piomelli, D. (2005) An endocannabinoid mechanism for stress-induced analgesia. Nature 435: 1108-1112.
  • Nackley, A.G., Zvonok, A.M., Makriyannis, A., and Hohmann, A.G. (2004) Activation of cannabinoid CB2 receptors suppresses C-fiber responses and windup in spinal wide dynamic range neurons in the absence and presence of inflammation. Journal of Neurophysiology 92: 3562-3574.
  • Nackley, A.G., Makriyannis, A. and Hohmann, A.G. (2003) Selective activation of cannabinoid CB2 receptors suppresses spinal Fos protein expression and pain behavior in a rat model of inflammation. Neuroscience 119: 747-757.