Study on dose-dependent, frequency-dependent, and accumulative effects of 1.5 GHz and 2.856 GHz microwave on cognitive functions in Wistar rats

Abstract

Many studies have revealed the cognitive decline induced by microwave radiation. However, the systematic study on dose-dependent, frequency-dependent and accumulative effects of microwave exposure at different frequencies was lacking. Here, we studied the relationship between the effects and the power and frequency of microwave and analyzed the accumulative effects of two different frequency microwaves with the same average power density. After microwave radiation, declines in spatial learning and memory and fluctuations of brain electric activities were found in the 10 mW/cm2 single frequency exposure groups and accumulative exposure groups. Meanwhile, morphological evidences in hippocampus also supported the cognitive dysfunction. Moreover, the decrease of Nissl contents in neurons indicated protein-based metabolic disorders in neurons. By detecting the key functional proteins of cholinergic transmitter metabolism, cytokines, energy metabolism and oxidative stress in the hippocampus, we found that microwave could lead to multiple metabolic disorders. Our results showed that microwave-induced cognitive decline was largely determined by its power rather than frequency. Injury effects were also found in accumulative exposure groups. We particularly concerned about the safety dose, injury effects and accumulative effects of microwaves, which might be very valuable in the future.

Acute radiofrequency electromagnetic radiation exposures cause neuronal DNA damage and impair neurogenesis in the young adolescent rat brain

“…Most of the damaged neurons have large vacuoles and are interspersed between normal neurons indicating damage happened in the living cells. These findings are in agreement with previous reports demonstrating neuronal degeneration in different brain regions after microwave exposure of varying frequencies, doses and durations (Bas et al, 2009; Odaci et al, 2008; Saikhedkar et al, 2014; Tan et al, 2017). Salford et al (2003) demonstrated prominent neuronal damage in cortex, hippocampus and basal ganglia by nonthermal microwave exposure of very low GSM signals (at a SAR of 0.002, 0.02 and 0.2 W/Kg) only for 2 h and sacrificed 50 days post irradiation.…”

Can Low-Level Exposure to Radiofrequency Fields Effect Cognitive Behaviour in Laboratory Animals? A Systematic Review of the Literature Related to Spatial Learning and Place Memory

“…Tan et al [27] compared the effects of single, acute exposure to two different frequencies on performance of rats in a Morris water maze task. Rats were exposed to either 1500 or 2856 MHz for 6 min or exposed to both frequencies for 6 min each at a whole-body SAR of 1.8 or 1.7 W/kg or at 3.7 or 3.3 W/kg.…”

Neurexin and Neuroligins Jointly Regulate Synaptic Degeneration at the Drosophila Neuromuscular Junction based on TEM Studies

“…Ultrastructural features of NMJ bouton degeneration in third instar Drosophila larva Synaptic degeneration can be caused by degenerative neurological diseases, such as Alzheimer's disease [51,52] and prion disease [13,24]; may also be caused by injuries, such as surgery, microwaves [20] and mild uid percussion [53]; or can occur in aging animals [15,22]. Fragmentation and degeneration of organelles exposes more proteins or polypeptides, which contain amino groups to which osmic acid can easily adsorb, resulting in electron density under an electron microscope.…”

“…Therefore, the stability of synaptic boutons is a dynamic balance among growth [12], pruning, degeneration, and elimination processes. Synapse degeneration is a complicated process that includes retraction [18,19] and degradation [14,20] of presynaptic and postsynaptic components, such as synaptic vesicles [13,15,19,[21][22][23], microtubules [2], and postsynaptic PSD [24]. Disordered elimination after synaptic degeneration can lead to autism [25] and other neurological diseases.…”

“…11B) [22], accompanied by reduction and fading of the presynaptic cytoskeletonassociated molecule Futsch [32,33] from distal boutons, which causes presynaptic contraction of the synapse and forms a synaptic footprint that has a smaller axon terminal and fewer synaptic vesicle signals [30,31]. Then, the T-bar detaches from the presynaptic membrane [50] with the swelling of mitochondria [20], some degenerating dark vesicles appear in the center of terminals, and the SSR further swells and retracts (Fig. 11 C).…”