| Autor: |
Macdonald, R L, Werz, M A |
| Zdroj: |
Journal of Physiology; August 1986, Vol. 377 Issue: 1 p237-249, 13p |
| Abstrakt: |
The actions of the opioid peptides dynorphin A and (Leu)enkephalin were assessed on calcium‐dependent action potentials and inward calcium currents recorded from somata of mouse dorsal root ganglion (d.r.g.) neurones grown in primary dissociated cell culture. Dynorphin A and (Leu)enkephalin decreased the duration of somatic calcium‐dependent action potentials in a portion of d.r.g. neurones impaled with potassium acetate‐filled micropipettes. When substantial potassium conductance was blocked by intracellular injection of caesium acetate, d.r.g. neurones continued to respond to dynorphin A but responses to (Leu)enkephalin were abolished. In voltage‐clamp experiments, dynorphin A but not (Leu)enkephalin reduced the magnitude of inward calcium currents. Dynorphin A responses were blocked by the opiate antagonist naloxone. The dynorphin A effect was due to reduction of voltage‐dependent calcium conductance since dynorphin A reduced depolarization‐evoked inward currents but did not alter membrane conductance following blockade of calcium channels by cadmium, and because dynorphin A reduced the instantaneous current‐voltage slope (chord conductance) during step commands that produced maximal activation of voltage‐dependent calcium conductance. Dynorphin A binds with high affinity to kappa‐opioid receptors. (Leu)enkephalin, which has affinity for both mu‐ and delta‐receptors but not for kappa‐opioid receptors, was without effect on calcium conductance. Therefore, we suggest that kappa‐receptors are coupled to voltage‐dependent calcium‐channels and that binding of dynorphin A produces a decrease of calcium current. |
| Databáze: |
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