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The Journal of Neuroscience, October 1, 1999, 19(19):8337-8348
 Opioid Receptor Modulation of Several Voltage-Dependent
Ca2+ Currents in Rat Sensory Neurons
Cristian G.
Acosta and
Héctor
S.
López
Instituto de Investigación Médica Mercedes y
Martín Ferreyra, Consejo Nacional de Investigaciones
Científicas y Técnicas, 5000 Córdoba, Argentina
Endogenous enkephalins and  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 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 (naltrindole, 1 µM), but not a µ ( -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 opioids could affect diverse Ca2+-dependent processes linked to
Ca2+ influx through different high-voltage-activated
channel types.
Key words:
Ca2+ channel; opioid receptor; modulation; sensory neuron; dorsal root ganglion; high-voltage-activated Ca2+ current; nimodipine;  -conotoxin GVIA; -agatoxin IVA; -conotoxin MVIIC
Copyright © 1999 Society for Neuroscience 0270-6474/99/19198337-12$05.00/0
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