Sex-dependent impact of perinatal 5G electromagnetic field exposure in the adolescent rat behavior.

The fifth generation (5G) network is currently being worldwide spread out, raising questions about the potential impact of this new technology, particularly on immature organisms. The current study aimed to investigate the effects of daily 5G electromagnetic field (EMF) perinatal exposure on the neurodevelopment of rats. The exposure level was set to the limit of whole-body public exposure defined by the International Commission on Non-Ionizing Radiation Protection. The mother rat specific absorption rate (SAR) was 0.07 W/kg for 22 h/day at 3500 MHz continuous wave from gestational day (GD) 8 to post-natal day (PND) 21. Clinical observations were performed on weight, length, sex ratio, number of pups per litter, and number of stillborn in sham and EMF-exposed groups (n = 7). The age of pinna ear detachment, incisor eruption, and eye opening were recorded. Behavior was assessed on righting, gripping, and negative geotaxis reflexes at PND 3 or 7 and on stereotyped and horizontal movements in the open field at PND 43. Our results indicated that both male and female pups showed delayed incisor eruption in the EMF-exposed group compared to the sham group (+ 1 day). Regarding activity in the open field, adolescent females showed less stereotyped movements (- 70%), while adolescent males showed more stereotyped movements (+ 50%) compared to the sham-exposed adolescent rats. Thus, the present study suggested that perinatal exposure to 5G at SAR level below reglementary threshold led to perturbations in the descendants seen in juveniles and adolescents.

The ephrin receptor EphB2 regulates the connectivity and activity of enteric neurons.

Highly organized circuits of enteric neurons are required for the regulation of gastrointestinal functions, such as peristaltism or migrating motor complex. However, the factors and molecular mechanisms that regulate the connectivity of enteric neurons and their assembly into functional neuronal networks are largely unknown. A better understanding of the mechanisms by which neurotrophic factors regulate this enteric neuron circuitry is paramount to understanding enteric nervous system (ENS) physiology. EphB2, a receptor tyrosine kinase, is essential for neuronal connectivity and plasticity in the brain, but so far its presence and function in the ENS remain largely unexplored. Here we report that EphB2 is expressed preferentially by enteric neurons relative to glial cells throughout the gut in rats. We show that in primary enteric neurons, activation of EphB2 by its natural ligand ephrinB2 engages ERK signaling pathways. Long-term activation with ephrinB2 decreases EphB2 expression and reduces molecular and functional connectivity in enteric neurons without affecting neuronal density, ganglionic fiber bundles, or overall neuronal morphology. This is highlighted by a loss of neuronal plasticity markers such as synapsin I, PSD95, and synaptophysin, and a decrease of spontaneous miniature synaptic currents. Together, these data identify a critical role for EphB2 in the ENS and reveal a unique EphB2-mediated molecular program of synapse regulation in enteric neurons.