title: Electromagnetic field effect or simply stress? Effects of UMTS exposure on hippocampal longterm plasticity in the context of procedure related hormone release.
abstract: Harmful effects of electromagnetic fields (EMF) on cognitive and behavioural features of humans and rodents have been controversially discussed and raised persistent concern about adverse effects of EMF on general brain functions. In the present study we applied radio-frequency (RF) signals of the Universal Mobile Telecommunications System (UMTS) to full brain exposed male Wistar rats in order to elaborate putative influences on stress hormone release (corticosteron; CORT and adrenocorticotropic hormone; ACTH) and on hippocampal derived synaptic long-term plasticity (LTP) and depression (LTD) as electrophysiological hallmarks for memory storage and memory consolidation. Exposure was computer controlled providing blind conditions. Nominal brain-averaged specific absorption rates (SAR) as a measure of applied mass-related dissipated RF power were 0, 2, and 10 W/kg over a period of 120 min. Comparison of cage exposed animals revealed, regardless of EMF exposure, significantly increased CORT and ACTH levels which corresponded with generally decreased field potential slopes and amplitudes in hippocampal LTP and LTD. Animals following SAR exposure of 2 W/kg (averaged over the whole brain of 2.3 g tissue mass) did not differ from the sham-exposed group in LTP and LTD experiments. In contrast, a significant reduction in LTP and LTD was observed at the high power rate of SAR (10 W/kg). The results demonstrate that a rate of 2 W/kg displays no adverse impact on LTP and LTD, while 10 W/kg leads to significant effects on the electrophysiological parameters, which can be clearly distinguished from the stress derived background. Our findings suggest that UMTS exposure with SAR in the range of 2 W/kg is not harmful to critical markers for memory storage and memory consolidation, however, an influence of UMTS at high energy absorption rates (10 W/kg) cannot be excluded.
authors.affiliation: Department of Neuroanatomy and Molecular Brain Research, Ruhr-University Bochum, Bochum, Germany.
authors.forename: Nora
authors.initials: N
authors.lastname: Prochnow
authors.forename: Tina
authors.initials: T
authors.lastname: Gebing
authors.forename: Kerstin
authors.initials: K
authors.lastname: Ladage
authors.forename: Dorothee
authors.initials: D
authors.lastname: Krause-Finkeldey
authors.forename: Abdessamad
authors.initials: A
authors.lastname: El Ouardi
authors.forename: Andreas
authors.initials: A
authors.lastname: Bitz
authors.forename: Joachim
authors.initials: J
authors.lastname: Streckert
authors.forename: Volkert
authors.initials: V
authors.lastname: Hansen
authors.forename: Rolf
authors.initials: R
authors.lastname: Dermietzel
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D003345:Corticosterone / Q000378:metabolism; D003863:Depression / Q000139:chemically induced; D004574:Electromagnetic Fields / Q000009:adverse effects*; D004594:Electrophysiology; D006624:Hippocampus / Q000378:metabolism* / Q000528:radiation effects*; D008297:Male; D009473:Neuronal Plasticity / Q000528:radiation effects*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000324:Adrenocorticotropic Hormone; D003345:Corticosterone