Release of tritiated agmatine from spinal synaptosomes

Cory J. Goracke-Postle, Hoang Oanh X. Nguyen, Laura S. Stone, Carolyn A. Fairbanks

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Intrathecal agmatine (decarboxylated arginine) moderates induction of neuropathic pain, spinal cord injury, and opioid tolerance in rodents. An endogenous central nervous system molecule and N-methyl-D-aspartate receptor antagonist/nitric oxide synthase inhibitor, agmatine may be a neuromodulator. We evaluated depolarization-induced release of agmatine from purified spinal nerve terminals (synaptosomes). Agmatine immunoreactivity was observed colocalized or closely apposed to some synaptophysin-and/or synaptotagmin-labeled structures. A temperature- and concentration-dependent uptake of [3H]-agmatine into synaptosomes was observed, consistent with an uptake mechanism. Potassium-induced depolarization resulted in release of [3H]- agmatine from the synaptosomes in a Ca2+-dependent manner, consistent with a neuromodulatory function. These results agree with previous reports of agmatine uptake into synaptosomes of the brain and extend those results to include stimulated release and a spinal site of activity.

Original languageEnglish (US)
Pages (from-to)13-17
Number of pages5
JournalNeuroreport
Volume17
Issue number1
DOIs
StatePublished - Jan 2006

Keywords

  • Arginine
  • Neuromodulator
  • Neurotransmitter
  • Polyamine
  • Spinal cord

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