Intracellular recordings were performed in vitro from dorsal root ganglion cell bodies isolated from adult rats. A- and C-type cells were distinguished according to the conduction velocity of their axons. Bath perfusion of normorphine, methionine-enkephalin (M-E) or [d-Ala2,d-Leu5]-enkephalin (DADL) did not alter membrane potential, threshold potential for spike initiation or the spike waveform either before or after addition of Ba2+ and 4-aminopyridine. Perfusion with γ-aminobutyric acid (GABA) depolarized A- and C-type cells and decreased input resistance. Picrotoxin antagonized this action. Morphine or M-E applied by perfusion never altered the GABA-induced depolarizations. Iontophoretically administered morphine reduced the GABA-induced depolarization without alteration of resting membrane properties or spike form, while M-E increased the GABA-induced depolarization. In about 50% of cells tested M-E applied iontophoretically produced a reversible hyperpolarization associated with an elevated input resistance (120-200% control). None of the effects produced by the opioids were antagonized by naloxone applied by perfusion or iontophoretically. These results suggest that the cell bodies of spinal ganglion cells of adult animals lack opiate receptors.
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