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Page 1
N-arachidonyl-glycine modulates synaptic transmission in superficial dorsal
horn*
Hyo-Jin Jeong*,1 2 1
, Robert J Vandenberg Christopher W Vaughan
1Pain Management Research Institute, Kolling Institute of Medical Research, Northern Clinical
School, University of Sydney at Royal North Shore Hospital, NSW, Australia; 2Department of
Pharmacology, Bosch Institute, University of Sydney, NSW, Australia.
Running title: NAGly enhances glycine transmission in dorsal horn
*Correspondence should be addressed to:
Dr Hyo-Jin Jeong
Pain Management Research Institute
Kolling Institute of Medical Research, Northern Clinical School
University of Sydney at Royal North Shore Hospital, St Leonards, NSW 2065, Australia
E-mail: jeong@.au Phone: +61-2-9926 4965. Fax: +61-2-9906 4079.
URL: .au
This is an Accepted Article that has been peer-reviewed and approved for
publication in the British Journal of Pharmacology, but has yet to undergo
copy-editing and proof correction. Please cite this article as an “Accepted
Article”; doi: 10.1111/j.1476-5381.2010.00935.x
Page 2
SUMMARY
Background and purpose. The arachidonyl-amino acid N-arachidonyl glycine (NAGly) is an endogenous
lipid, generated within the spinal cord and producing spinally mediated analgesia via non-cannabinoid
mechanisms. In this study we examined the actions of NAGly on neurons within the superficial dorsal
horn, a key site for the actions of many analgesic agents.
Experimental approach. Whole cell patch clamp recordings were made from lamina II neurons in rat
spinal cord slices to examine the effect of NAGly on glycinergic and NMDA-mediated synaptic
transmission.
Key results. NAGly prolonged the decay of glycine, but
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