Abstract
The opioid receptors have been considered one of the mechanisms by which the analgesic effects of 30-min exposures to temporally patterned weak (1 mT) magnetic fields are mediated. In 3 separate blocks of experiments, we explored the interactions between 2 examples of these magnetic fields as well as compounds that influence L-type calcium (nimodipine) channels, dopamine D2 receptors (haldol, chlorpromazine), and glucocorticoid receptors (prednisolone). Nimodipine produced a mild analgesic response that was reduced by exposure to a theta burst pattern and which did not produce analgesia by itself, but is known to produce long-term potentiation in hippocampal slices. The analgesia evoked by the burst-firing field was not reduced by nimodipine. Neither of the D2 antagonists nor prednisolone produced significant analgesia nor blocked the analgesic effects produced by the burst-firing field.