Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 8 November 2005
Vol. 2005, Issue 309, p. pe51
[DOI: 10.1126/stke.3092005pe51]

PERSPECTIVES

Endocannabinoid Identification in the Brain: Studies of Breakdown Lead to Breakthrough, and There May Be NO Hope

Bradley E. Alger*

Departments of Physiology and Psychiatry, Program in Neuroscience, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Abstract: Endocannabinoids are a class of fatty acid derivatives defined by their ability to interact with the specific cannabinoid receptors that were originally identified as the targets of {Delta}9-tetrahydocannabinol ({Delta}9-THC), the psychoactive component of cannabis. Endocannabinoids have been implicated in a growing number of important physiological and behavioral events. A full understanding of the functions of endocannabinoids will involve knowing which ones are active, and how they are produced, during any given physical event. However, studying these small lipids in the brain presents many technical challenges. New selective pharmacological tools promise to be very useful in unraveling the complexities of endocannabinoid signaling, but parallel developments from the investigation of the cellular neurophysiology of the endocannabinoid systems highlight the difficulties remaining.

*Contact information. Telephone, 410-706-3350; fax, 410-706-8341; e-mail, balger{at}umaryland.edu

Citation: B. E. Alger, Endocannabinoid Identification in the Brain: Studies of Breakdown Lead to Breakthrough, and There May Be NO Hope. Sci. STKE 2005, pe51 (2005).

Read the Full Text

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Genetic deletion of monoacylglycerol lipase alters endocannabinoid-mediated retrograde synaptic depression in the cerebellum.
P. Zhong, B. Pan, X.-p. Gao, J. L. Blankman, B. F. Cravatt, and Q.-s. Liu (2011)
J. Physiol. 589, 4847-4855
   Abstract »    Full Text »    PDF »
Alterations of Endocannabinoid Signaling, Synaptic Plasticity, Learning, and Memory in Monoacylglycerol Lipase Knock-out Mice.
B. Pan, W. Wang, P. Zhong, J. L. Blankman, B. F. Cravatt, and Q.-s. Liu (2011)
J. Neurosci. 31, 13420-13430
   Abstract »    Full Text »    PDF »
D2 Dopamine Receptor Activation Facilitates Endocannabinoid-Mediated Long-Term Synaptic Depression of GABAergic Synaptic Transmission in Midbrain Dopamine Neurons via cAMP-Protein Kinase A Signaling.
B. Pan, C. J. Hillard, and Q.-s. Liu (2008)
J. Neurosci. 28, 14018-14030
   Abstract »    Full Text »    PDF »
Endocannabinoid Signaling Mediates Cocaine-Induced Inhibitory Synaptic Plasticity in Midbrain Dopamine Neurons.
B. Pan, C. J. Hillard, and Q.-s. Liu (2008)
J. Neurosci. 28, 1385-1397
   Abstract »    Full Text »    PDF »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882