This animal study examined whether paternal exposure to 4.9 GHz (5G) radiofrequency radiation affects male offspring in C57BL/6 mice. It reports increased anxiety-like behavior and reduced sperm quality in adult F1 males from exposed fathers, alongside reported LRGUK hypermethylation and reduced LRGUK expression in testes. The abstract reports no significant effects on depression-like behavior, learning/memory, or fertility across F1–F2 generations.

This animal study examined repeated asymmetrical head exposure to a 5G-modulated 3.5 GHz signal in adult male mice for six weeks. It reports no significant changes in locomotion, anxiety, or object-based memory performance under the tested conditions. However, it found statistically significant but limited cortical gene expression changes (<1% of expressed genes), including enrichment for glutamatergic synapse-related genes and lateralized differences involving mitochondrial genome-encoded genes. The authors caution that potential health risks from these intracortical transcriptomic modifications should not be downplayed and note uncertainties about longer exposures and other populations.

This animal study examined repeated pulsed-modulated RF exposure (1–4 GHz; total pulse power density 300 μW/cm2) in male and female Wistar rats and assessed behavior using the open field test. The abstract reports stress reactions and long-term memory impairment in some rats, with females described as more sensitive than males. Reported effects were transient, with behavior returning to baseline within 1.5–2 months after exposure stopped. The authors suggest potential concern for constant exposure scenarios, though this is not directly evaluated in humans here.

This animal study exposed 108 male Sprague-Dawley rats to 900 MHz EMF (1 mW/cm2) or sham for 14 or 28 days (3 h/day). The authors report that 28-day exposure was associated with impaired spatial memory, BBB permeability damage, and ultrastructural changes in hippocampus and cortex. They also report increased mkp-1 expression and ERK dephosphorylation, proposing activation of the mkp-1/ERK pathway as a mechanism.