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 Previous Article
Journal of Neuroscience, Vol 13, 867-873, Copyright © 1993 by Society for Neuroscience
Inhibition of Ca2+ currents by a mu-opioid in a defined subset of rat sensory neurons
JE Schroeder and EW McCleskey
Department of Cell Biology and Physiology, Washington University, St. Louis, Missouri 63110.
Activation of the endogenous opioid system can suppress pain without
affecting other sensations, but the cellular mechanism of this selectivity
is unclear. The analgesia might be due to inhibitory synapses arranged only
on neurons whose activity leads to pain sensations. Alternatively, opioids
might be released broadly, with neurons involved in pain sensation being
especially sensitive. Therefore, we asked whether different subsets of rat
dorsal root ganglion (DRG) sensory neurons vary in their sensitivity to
opioids. Dissociated neurons were subdivided according to the spinal
laminae to which they likely had projected, and whether they had innervated
muscle. Using the patch-clamp method, we measured the inhibition of Ca2+
current by DAGO (Tyr-D-Ala-Gly-MePhe-Gly-ol), a peptide that selectively
activates the mu (morphine) receptor. We also investigated the presence of
different types of Ca2+ channels. In DRG neurons chosen at random, Ca2+
currents were inhibited by DAGO to widely varying degrees, with an average
inhibition of 38%. Ca2+ currents in neurons in a subset that projects to
laminae I and II had a lower average inhibition, and unlike the randomly
selected cells, the responses were predictable and tightly distributed
about the mean. This indicates that the variability of opioid sensitivity
among DRG neurons reflects the presence of different subsets of cells.
Since neurons projecting to laminae I and II, the projection site of
nociceptive neurons, did not show high opioid sensitivity, there is no
evidence that nociceptive neurons have stronger responses to opioids. But a
firm conclusion is impossible because projection site does not strictly
define sensory modality.
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