Hyperactivity caused by a nitric oxide synthase inhibitor is countered by ultra-wideband pulses

Abstract

Potential action of ultra‐wideband (UWB) electromagnetic field pulses on effects of NG‐nitro‐ L‐arginine methyl ester (L‐NAME), an inhibitor of nitric oxide synthase (NOS), on nociception and locomotor activity was investigated in CF‐1 mice. Animals were injected IP with saline or 50 mg/kg L‐NAME and exposed for 30 min to no pulses (sham exposure) or UWB pulses with electric field parameters of 102±1 kV/m peak amplitude, 0.90±0.05 ns duration, and 160±5 ps rise time (mean±S.D.) at 600/s. Animals were tested for thermal nociceptive responses on a 50°C surface and for spontaneous locomotor activity for 5 min. L‐NAME by itself increased mean first‐response (paw lift, shake, or lick; jump) and back‐paw‐lick response latencies and mean locomotor activity. Exposure to UWB pulses reduced the L‐NAME–induced increase in back‐paw‐lick latency by 22%, but this change was not statistically significant. The L‐NAME–induced hyperactivity was not present after UWB exposure. Reduction and cancellation of effects of L‐NAME suggest activation of opposing mechanism(s) by the UWB pulses, possibly including increase of nitric oxide production by NOS. The action, or actions, of UWB pulses appears to be more effective on locomotor activity than on thermal nociception in CF‐1 mice. Bioelectromagnetics 20:431–439, 1999. © 1999 Wiley‐Liss, Inc.

BEHAVIORAL EFFECTS OF COMBINED PERINATAL L-NAME AND 0.5 Hz MAGNETIC FIELD TREATMENTS

“…However, residual changes in baseline motor activity (as inferred by the numbers of midline chamber crossovers prior to context/shock pairings during the contextual fear conditioning paradigm) and for latencies to respond to thermal stimuli, were evident. Although motor activity and thermal analgesia are both affected by acute L-NAME administration, the vector of the effect appears to be influenced by animal strain (Seaman, Belt, Doyle, & Mathur, 1999). For instance, Moore, Oluyomi, Babbedge, Wallace, & Hart (1991) have reported that acute NOS inhibition dose-dependently (1-75 mg/kg) increased latencies in the formalin pain test while large doses of L-NAME (600 mg/kg) reduced baseline motor activity.…”

“…For instance, Moore, Oluyomi, Babbedge, Wallace, & Hart (1991) have reported that acute NOS inhibition dose-dependently (1-75 mg/kg) increased latencies in the formalin pain test while large doses of L-NAME (600 mg/kg) reduced baseline motor activity. Seaman et al (1999) have demonstrated that the thermal latency (to back paw licks) following 50 mg/kg L-NAME increased by approximately 100% relative to untreated mice. This same dose of L-NAME increased motor activity (assessed by light beam interruptions in an open field environment) by approximately 20% relative to untreated mice.…”

“…Although the augmentation of thermal antinociception by L-NAME treatments in the Wistar rat has been demonstrated (Dixon & Persinger, 2001), the effects of this treatment on baseline motor activity in this strain have not. In the context of the findings reported by Seaman et al (1999) that L-NAME increased both thermal latencies and baseline motor activity (and given that termination of chronic L-NAME and magnetic field treatment in the present study may have caused a nitric oxide rebound) the findings of chronic suppressions in motor activity and decreased thermal latencies may suggest a long-term but subtle overshoot in nitric oxide activity (e.g., a long-term upregulation of nitric oxide synthase activity). The ontogenetic enhancement of neurotransmitter activity, such as dopamine with the corpus striatum, has been reported for rats exposed prenatally to more intense (50 mT) static magnetic fields (Lee et al, 2001).…”

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“…While L-NAME was capable of inducing increased spontaneous activity in sham exposed mice, its effect was blocked entirely by the UWB exposure. In supporting the evidence that UWB pulses could affect nitric oxide production, Seaman et al [1999] referred to an enhanced nitric oxide production by 41 % in stimulated murine macrophages incubated with potassium nitrate (GLN treatment) after UWB exposure ]. The nitric oxide produced was 9.14 mM in sham-exposed and 12.89 mM in UWB-exposed GLN treated macrophages.…”

“…In an extension of their original study on morphine and UWB, Seaman et al [1999] studied the effects of a NOS inhibitor, N°-nitro-L-arginine methyl ester (L-NAME) on manifestation of UWB effects in CF-lTPlus. mice.…”