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Published on: October 27, 2020
Involvement of NMDA receptor in low-frequency magnetic field-induced anxiety in mice
Balwant P Salunke1, Sudhir N Umathe, Jagatpalsingh G Chavan
1Department of Pharmaceutical Sciences, Rashtrasant Tukadoji Maharaj Nagpur University, Mahatma Jyotiba Fuley Shaikshanik Parisar , Nagpur, Maharashtra , India.
Abstract:
It had been reported that exposure to extremely low-frequency magnetic field (ELFMF) induces anxiety in human and rodents. Anxiety mediates via the activation of N-methyl-d-aspartate (NMDA) receptor, whereas activation of γ-aminobutyric acid (GABA) receptor attenuates the same. Hence, the present study was carried out to understand the contribution of NMDA and/or GABA receptors modulation in ELFMF-induced anxiety for which Swiss albino mice were exposed to ELFMF (50 Hz, 10 G) by subjecting them to Helmholtz coils. The exposure was for 8 h/day for 7, 30, 60, 90 and 120 days. Anxiety level was assessed in elevated plus maze, open field test and social interaction test, on 7th, 30th, 60th, 90th and 120th exposure day, respectively. Moreover, the role of GABA and glutamate in ELFMF-induced anxiety was assessed by treating mice with muscimol [0.25 mg/kg intraperitoneally (i.p.)], bicuculline (1.0 mg/kg i.p.), NMDA (15 mg/kg i.p.) and MK-801 (0.03 mg/kg i.p.), as a GABAA and NMDA receptor agonist and antagonist, respectively. Glutamate receptor agonist exacerbated while inhibitor attenuated the ELFMF-induced anxiety. In addition, levels of GABA and glutamate were determined in regions of the brain viz, cortex, striatum, hippocampus and hypothalamus. Experiments demonstrated significant elevation of GABA and glutamate levels in the hippocampus and hypothalamus. However, GABA receptor modulators did not produce significant effect on ELFMF-induced anxiety and elevated levels of GABA at tested dose. Together, these findings suggest that ELFMF significantly induced anxiety behavior, and indicated the involvement of NMDA receptor in its effect.
Insights
Extremely low-frequency magnetic field (ELFMF) exposure induced anxiety in mice, primarily involving N-methyl-d-aspartate (NMDA) receptors. Gamma-aminobutyric acid (GABA) receptor modulation did not significantly affect this ELFMF-induced anxiety.
Area of Science:
- Neuroscience
- Environmental Health
- Toxicology
Background:
- Extremely low-frequency magnetic fields (ELFMF) are increasingly prevalent, with prior reports suggesting their link to anxiety in humans and rodents.
- Anxiety is modulated by neurotransmitter systems, specifically the excitatory N-methyl-d-aspartate (NMDA) receptor and the inhibitory gamma-aminobutyric acid (GABA) receptor.
Purpose of the Study:
- To investigate the contribution of NMDA and GABA receptor modulation in anxiety induced by ELFMF exposure.
- To assess the behavioral and neurochemical changes associated with prolonged ELFMF exposure in a rodent model.
Main Methods:
- Swiss albino mice were exposed to ELFMF (50 Hz, 10 G) for 8 hours daily over periods of 7 to 120 days.
- Anxiety levels were evaluated using behavioral tests: elevated plus maze, open field test, and social interaction test.
- The roles of GABA and glutamate receptors were examined by administering specific agonists and antagonists (muscimol, bicuculline, NMDA, MK-801), and neurotransmitter levels were measured in brain regions.
Main Results:
- ELFMF exposure induced significant anxiety-like behavior in mice across various exposure durations.
- NMDA receptor agonists exacerbated, while antagonists attenuated, ELFMF-induced anxiety.
- Significant elevations in both GABA and glutamate levels were observed in the hippocampus and hypothalamus, though GABA receptor modulators showed no significant effect on anxiety or GABA levels.
Conclusions:
- ELFMF exposure is a significant inducer of anxiety behavior in mice.
- The findings strongly indicate the involvement of the NMDA receptor pathway in mediating ELFMF-induced anxiety.
- GABAergic system modulation does not appear to be the primary mechanism underlying ELFMF-induced anxiety at the tested doses.

