Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form

The enzymatic inactivation of the fatty acid amide class of signaling lipids

Academic Article
uri icon
  • Overview
  • Research
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Cravatt, Benjamin
  • Lichtman, A. H.

publication date

  • December 2002

journal

  • Chemistry and Physics of Lipids  Journal

abstract

  • The fatty acid amide (FAA) class of signaling lipids modulates a number of neurobehavioral processes in mammals, including pain, sleep, feeding, and locomotor activity. Representative FAAs include the endogenous cannabinoid anandamide and the sleep-inducing lipid oleamide. Despite activating several neuroreceptor systems in vitro, most FAAs produce only weak and transient behavioral effects in vivo, presumably due to their expeditious catabolism. This review focuses on one enzyme, fatty acid amide hydrolase (FAAH) that appears to play a major role in regulating the amplitude and duration of FAA signals in vivo. In particular, we will highlight a series of recent papers that have investigated the physiological functions of the mouse and human FAAH enzymes. Collectively, these studies promote FAAH as a central component of FAA signaling pathways, especially those mediated by the endocannabinoid anandamide, and suggest that this enzyme may represent an attractive pharmaceutical target for the treatment of pain and related neurophysiological disorders.

subject areas

  • Amides
  • Amidohydrolases
  • Amino Acid Sequence
  • Animals
  • Arachidonic Acids
  • Cannabinoid Receptor Modulators
  • Cannabinoids
  • Endocannabinoids
  • Fatty Acids
  • Humans
  • Polyunsaturated Alkamides
  • Signal Transduction
  • Synapses
scroll to property group menus

Research

keywords

  • anandamide
  • endocannabinoid
  • fatty acid amide hydrolase
  • oleamide
  • pain
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0009-3084

Digital Object Identifier (DOI)

  • 10.1016/s0009-3084(02)00147-0

PubMed ID

  • 12505696
scroll to property group menus

Additional Document Info

start page

  • 135

end page

  • 148

volume

  • 121

issue

  • 1-2

©2021 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support