cAMP decreases steady-state levels of delta-opioid receptor mRNA in NG108-15 cells

Neuroreport. 1997 Jul 7;8(9-10):2369-72. doi: 10.1097/00001756-199707070-00053.


We have compared several drug combinations for their ability to increase basal cAMP and to down-regulate delta-opioid receptor mRNA levels. Continuous treatment for up to 48 h with a phosphodiesterase inhibitor in combination with the adenylyl cyclase activator forskolin showed an early peak response, but cAMP levels returned to control after 8 and 24 h. Increases in cAMP level up to 150-fold were observed after treatment for 1 h with a series of drugs (rolipram, IBMX/forskolin, rolipram/forskolin, dibutyryl cAMP, and prostaglandin E2) that increase cAMP by different mechanisms. A significant decrease in DOR mRNA level, to 31% of control, followed the three treatments that produced the largest increases in cAMP level: IBMX/forskolin, rolipram/forskolin, and prostaglandin E2.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 1-Methyl-3-isobutylxanthine / pharmacology
  • Animals
  • Colforsin / pharmacology
  • Cyclic AMP / metabolism*
  • Dinoprostone / pharmacology
  • Neuroblastoma / metabolism
  • Phosphodiesterase Inhibitors / pharmacology*
  • Pyrrolidinones / pharmacology
  • RNA, Messenger / metabolism
  • Receptors, Opioid, delta / drug effects
  • Receptors, Opioid, delta / metabolism*
  • Rolipram


  • Phosphodiesterase Inhibitors
  • Pyrrolidinones
  • RNA, Messenger
  • Receptors, Opioid, delta
  • Colforsin
  • Cyclic AMP
  • Rolipram
  • Dinoprostone
  • 1-Methyl-3-isobutylxanthine