Morphine modulates nociceptive transmission at the level of the spinal cord through opioid receptors localized pre-and post-synaptically on primary afferent fibers and dorsal horn neurons, respectively. We determined previously that morphine inhibited the depolarization-evoked increase in intracellular Ca2+ in the cell body of dissociated, adult dorsal root ganglion (DRG) neurons, and that this effect was mediated by µ- (MOR) and δ- (DOR) opioid receptors (Khasabova et al., SFN abstract #453.2, 2002). The present study used the same model to address which opioid receptors modulate K+-evoked release of calcitonin gene-related peptide (CGRP) from DRG neurons in vitro. Pretreatment of DRG neurons with morphine (1 mM) decreased K+- evoked CGRP release by 40%. The inhibitory effect of morphine was blocked by naltrindole (100 nM), a selective DOR antagonist, and was insensitive to CTAP (3nM – 100nM), a selective MOR antagonist. Naltrindole and CTAP alone had no effect. Examination of immunostained spinal cord se...