Nature Neuroscience
- 8, 1139 - 1141 (2005)
Published online: 7 August 2005; Corrected online: 12 December 2006 | doi:10.1038/nn1521
There is a Corrigendum (January 2007) associated with this Brief Communication.
Selective inhibition of 2-AG hydrolysis enhances endocannabinoid signaling in hippocampusJudit K Makara1, Marco Mor2, Darren Fegley3, 5, Szilárd I Szabó1, Satish Kathuria3, 5, Giuseppe Astarita3, 5, Andrea Duranti4, Andrea Tontini4, Giorgio Tarzia4, Silvia Rivara2, Tamás F Freund1 & Daniele Piomelli3, 51
Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, 8. Szigony u. 43., Budapest, H-1083 Hungary. 2
Pharmaceutical Department, University of Parma, Parco Area delle Scienze, 27/A, Parma, I-43100 Italy. 3
Department of Pharmacology, University of California Irvine, Irvine, California 92697-4625, USA. 4
Institute of Medicinal Chemistry, University of Urbino 'Carlo Bo', Piazza del Rinascimento, 6, Urbino, I-61029, Italy. 5
Center for Drug Discovery, University of California Irvine, Irvine, California 92697-4625, USA.
Correspondence should be addressed to Daniele Piomelli piomelli@uci.edu or Tamás F Freund freund@koki.hu The functions of 2-arachidonoylglycerol (2-AG), the most abundant endocannabinoid found in the brain, remain largely unknown. Here we show that two previously unknown inhibitors of monoacylglycerol lipase, a presynaptic enzyme that hydrolyzes 2-AG, increase 2-AG levels and enhance retrograde signaling from pyramidal neurons to GABAergic terminals in the hippocampus. These results establish a role for 2-AG in synaptic plasticity and point to monoacylglycerol lipase as a possible drug target.
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