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Electromagnetic Fields in Biological Systems
human volunteers, leaving pain perception unchanged (Kovács-Bálint et al., 2011). They
speculated that SMF-induced peripheral neuronal or circulatory mechanisms may be
involved in the observed TPT increase by setting the pain fiber adaptation potential to
higher levels.
Many studies have demonstrated that ELF-EMFs may be involved in hyperalgesia.
Jeong, Choi, Moon, et al. (2005) suggested that an ELF-EMF (60 Hz, 2.5 mT) can produce hyperalgesia and such a response can be regulated by the benzodiazepine system in
rats. Diazepam (a benzodiazepine receptor agonist), flumazenil (a benzodiazepine receptor antagonist), or both were used with EMF exposure. When testing the pain threshold
of rats using hot plate tests, EMF or diazepam was found to induce hyperalgesic effects
with a reduction in latency. These effects were blocked by pretreatment with flumazenil.
When the rats were exposed simultaneously to EMF and diazepam, the latency tended
to decrease without statistical significance. The induction of hyperalgesia by coexposure to EMF and diazepam was also blocked by flumazenil. However, pretreatment by
γ-aminobutyric acid (GABA) receptor antagonists such as bicuculline (a GABA A antagonist) or phaclofen (a GABA B antagonist) did not antagonize the hyperalgesic effect of
EMF. These results suggest that the benzodiazepine system may be involved in EMFinduced hyperalgesia. The same research group later suggested that the ELF-EMF might
cause Ca 2+ -dependent NOS activation, which then induces hyperalgesia with an increase
in NO synthesis in mice (Jeong et al. 2006). They concluded that ELF-EMF may produce
hyperalgesia by modulating NO synthesis via Ca 2+ -dependent NOS.
Bao et al. (2006) investigated the analgesic effect of an ELF-EMF (55.6 Hz, 8.1 mT)
in rats. The authors found that tail-flick latencies (TFLs) increased significantly after
exposure (6 h/day for 4 days). The analgesic effects seemed to decrease gradually when
the rats were exposed daily for another 10 days. The levels of TFL decreased in 1 day
when the rats were removed after a 4-day exposure. The concentrations of hypothalamus
β-endorphin, substance P, and brain stem serotonin (5-HT) were found significantly
increased on day 4. However, no differences were found when the rats were exposed for
another 10 days, and there were no significant increases when rats were removed after
the fourth day of exposure and tested for nociception on days 5 and 7 with no changes
in biochemical markers at 7 days. These results suggest that ELF-EMFs have an analgesic
effect, but only on days 3 and 4. The authors speculated that the EMF effect may be associated with increases in endogenous β-endorphin, substance P, and 5-HT.
Mert, Gunay, and Ocal (2010) examined the efficacy of PEMF (1, 10, 20, and 40 Hz;
1.5 mT; 1 h/day for 4 weeks) on diabetic neuropathy in streptozotocin (STZ)-induced
acute (3 days) and chronic (6 weeks) diabetic rats. After STZ administration, blood glucose levels elevated and body weights decreased in the studied rats. Although PEMF
treatment did not affect changes in body weight, the blood glucose levels of PEMFtreated diabetic rats exhibited a decrease during the treatments. Diabetic animals displayed marked decreases in mechanical thresholds and thermal latencies. Whereas
treatment with PEMF partially restored the mechanical threshold and thermal latency
in acute diabetic rats, PEMF had a corrective effect only on the mechanical threshold of
chronic diabetic rats. These results suggested that treatment with PEMF can potentially
ameliorate the painful symptoms of diabetes, such as hyperalgesia and allodynia, by
partially preventing hyperglycemia.
Electromagnetic Fields in Biological Systems
human volunteers, leaving pain perception unchanged (Kovács-Bálint et al., 2011). They
speculated that SMF-induced peripheral neuronal or circulatory mechanisms may be
involved in the observed TPT increase by setting the pain fiber adaptation potential to
higher levels.
Many studies have demonstrated that ELF-EMFs may be involved in hyperalgesia.
Jeong, Choi, Moon, et al. (2005) suggested that an ELF-EMF (60 Hz, 2.5 mT) can produce hyperalgesia and such a response can be regulated by the benzodiazepine system in
rats. Diazepam (a benzodiazepine receptor agonist), flumazenil (a benzodiazepine receptor antagonist), or both were used with EMF exposure. When testing the pain threshold
of rats using hot plate tests, EMF or diazepam was found to induce hyperalgesic effects
with a reduction in latency. These effects were blocked by pretreatment with flumazenil.
When the rats were exposed simultaneously to EMF and diazepam, the latency tended
to decrease without statistical significance. The induction of hyperalgesia by coexposure to EMF and diazepam was also blocked by flumazenil. However, pretreatment by
γ-aminobutyric acid (GABA) receptor antagonists such as bicuculline (a GABA A antagonist) or phaclofen (a GABA B antagonist) did not antagonize the hyperalgesic effect of
EMF. These results suggest that the benzodiazepine system may be involved in EMFinduced hyperalgesia. The same research group later suggested that the ELF-EMF might
cause Ca 2+ -dependent NOS activation, which then induces hyperalgesia with an increase
in NO synthesis in mice (Jeong et al. 2006). They concluded that ELF-EMF may produce
hyperalgesia by modulating NO synthesis via Ca 2+ -dependent NOS.
Bao et al. (2006) investigated the analgesic effect of an ELF-EMF (55.6 Hz, 8.1 mT)
in rats. The authors found that tail-flick latencies (TFLs) increased significantly after
exposure (6 h/day for 4 days). The analgesic effects seemed to decrease gradually when
the rats were exposed daily for another 10 days. The levels of TFL decreased in 1 day
when the rats were removed after a 4-day exposure. The concentrations of hypothalamus
β-endorphin, substance P, and brain stem serotonin (5-HT) were found significantly
increased on day 4. However, no differences were found when the rats were exposed for
another 10 days, and there were no significant increases when rats were removed after
the fourth day of exposure and tested for nociception on days 5 and 7 with no changes
in biochemical markers at 7 days. These results suggest that ELF-EMFs have an analgesic
effect, but only on days 3 and 4. The authors speculated that the EMF effect may be associated with increases in endogenous β-endorphin, substance P, and 5-HT.
Mert, Gunay, and Ocal (2010) examined the efficacy of PEMF (1, 10, 20, and 40 Hz;
1.5 mT; 1 h/day for 4 weeks) on diabetic neuropathy in streptozotocin (STZ)-induced
acute (3 days) and chronic (6 weeks) diabetic rats. After STZ administration, blood glucose levels elevated and body weights decreased in the studied rats. Although PEMF
treatment did not affect changes in body weight, the blood glucose levels of PEMFtreated diabetic rats exhibited a decrease during the treatments. Diabetic animals displayed marked decreases in mechanical thresholds and thermal latencies. Whereas
treatment with PEMF partially restored the mechanical threshold and thermal latency
in acute diabetic rats, PEMF had a corrective effect only on the mechanical threshold of
chronic diabetic rats. These results suggested that treatment with PEMF can potentially
ameliorate the painful symptoms of diabetes, such as hyperalgesia and allodynia, by
partially preventing hyperglycemia.