Release of calcitonin gene-related peptide like-immunoreactivity induced by electrical field stimulation from rat spinal afferents is mediated by conotoxin-sensitive calcium channels

Abstract

Electrical field stimulation (EFS, 10 V, 50 mA/cm 2, 5–50 Hz, 1 ms pulse duration, 10 s train every 20 s for 5 min) produced a rapid and reproducible outflow of calcitonin gene-related peptide like-immunoreactivity (CGRP-LI) from superfused slices from the dorsal half of the rat spinal cord which is abolished by tetrodotoxin (TTX, 0.3 μM), in vitro capsaicin desensitization (10 μM for 30 min) and in Ca-free medium. The response was unaffected by ruthenium red (10 μM), indomethacin (10 μM) and nifedipine (1 μM) while it was abolished by ω-conotoxin (ω-CTX, 0.1 μM) and, in a naloxone-sensitive manner, by morphine (3 μM). Since CGRP release from capsaicin-sensitive afferents evoked by EFS in rat peripheral tissues is conotoxin-resistant, these findings provide direct evidence for a qualitative difference between central and peripheral endings of capsaicin-sensitive primary afferents in the mechanisms regulating transmitter release in the same species.