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Endogenous enkephalins and δ opiates affect sensory function and pain sensation by inhibiting synaptic transmission in sensory circuits via delta opioid receptors (DORs). DORs have long been suspected of mediating these effects by modulating voltage-dependent Ca2+ entry in primary sensory neurons. However, not only has this hypothesis never been validated in these cells, but in fact several previous studies have only turned up negative results. By using whole-cell current recordings, we show that the δ enkephalin analog [d-Ala2,d-Leu5]-enkephalin (DADLE) inhibits, via DORs, L-, N-, P-, and Q-high voltage-activated Ca2+ channel currents in cultured rat dorsal root ganglion (DRG) neurons. The percentage of responding cells was remarkably high (75%) within a novel subpopulation of substance P-containing neurons compared with the other cells (18–35%). DADLE (1 μm) inhibited 32% of the total barium current through calcium channels (IBa). A δ (naltrindole, 1 μm), but not a μ (β-funaltrexamine, 5 μm), antagonist prevented the DADLE response, whereas a DOR-2 subtype (deltorphin-II, 100 nm), but not a DOR-1 (DPDPE, 1 μm), agonist mimicked the response. L-, N-, P-, and Q-type currents contributed, on average, 18, 48, 14, and 16% to the total IBa and 19, 50, 26, and 20% to the DADLE-sensitive current, respectively. The drug-insensitive R-type current component was not affected by the agonist. This work represents the first demonstration that DORs modulate Ca2+entry in sensory neurons and suggests that δ opioids could affect diverse Ca2+-dependent processes linked to Ca2+ influx through different high-voltage-activated channel types.

δ Opioid Receptor Modulation of Several Voltage-Dependent Ca2+Currents in Rat Sensory Neurons

δ Opioid Receptor Modulation of Several Voltage-Dependent Ca²⁺Currents in Rat Sensory Neurons