Sustained cannabinoid agonist treatment augments CGRP release in a PKA-dependent manner

Suneeta Tumati, Henry I. Yamamura, Paul A. St John, Todd W. Vanderah, William R. Roeske, Eva V. Varga

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


Studies have shown that sustained cannabinoid treatment increases the sensitivity to painful heat stimuli (thermal hyperalgesia) and innocuous mechanical stimuli (tactile allodynia). It has been suggested that augmented release of pain neurotransmitters (such as calcitonin gene-related peptide, CGRP) might be responsible for this abnormal pain sensitization. We hypothesize that intracellular adaptations upon sustained cannabinoid treatment causes augmented release of CGRP from primary nociceptors leading to increased pain sensitivity. We show that sustained (24h) cannabinoid agonist [(+)WIN 55,212-2] treatment of 7-day-old neonatal rat dorsal root ganglion neurons significantly augments basal CGRP release from these cells in a protein kinase A-dependent manner. Our results indicate that these intracellular compensatory adaptations may play a crucial trigger role in further neuronal system adaptations for modulation of pain.

Original languageEnglish (US)
Pages (from-to)815-819
Number of pages5
Issue number8
StatePublished - May 27 2009


  • 212-2
  • AM 251
  • Calcitonin gene-related peptide
  • Cannabinoids
  • Dorsal root ganglion neurons
  • WIN 55

ASJC Scopus subject areas

  • Neuroscience(all)


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