Electromagnetic Field Effect or Simply Stress? Effects of UMTS Exposure on Hippocampal Longterm Plasticity in the Context of Procedure Related Hormone Release

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

By Regulating Mitochondrial Ca2+-Uptake UCP2 Modulates Intracellular Ca2+.

The possible role of UCP2 in modulating mitochondrial Ca2+-uptake (mCa2+-uptake) via the mitochondrial calcium uniporter (MCU) is highly controversial.Thus, we analyzed mCa2+-uptake in isolated cardiac mitochondria, MCU single-channel activity in cardiac mitoplasts, dual Ca2+-transients from mitochondrial ((Ca2+)m) and intracellular compartment ((Ca2+)c) in the whole-cell configuration in cardiomyocytes of wild-type (WT) and UCP2-/- mice.Isolated mitochondria showed a Ru360 sensitive mCa2+-uptake, which was significantly decreased in UCP2-/- (229.4±30.8 FU vs. 146.3±23.4 FU, P0.05) and transsarcolemmal Ca2+-influx was inhibited suggesting a possible compensatory mechanism. Additionally, we observed an inhibitory effect of ATP on mCa2+-uptake in WT mitoplasts and (Ca2+)m of cardiomyocytes leading to an increase of (Ca2+)c while no ATP dependent effect was observed in UCP2-/-.Our results indicate regulatory effects of UCP2 on mCa2+-uptake. Furthermore, we propose, that previously described inhibitory effects on MCU by ATP may be mediated via UCP2 resulting in changes of excitation contraction coupling

Electromagnetic field effect or simply stress? Effects of UMTS exposure on hippocampal longterm plasticity in the context of procedure related hormone release

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

By Regulating Mitochondrial Ca²⁺-Uptake UCP2 Modulates Intracellular Ca²⁺ - Fig 3

a-c) Ca2+ transients in wild-type (WT) and in UCP2-/- cardiomyocytes (UCP2). a-b) Statistical analysis of (Ca2+)c (left) and (Ca2+)m (right) and c) representative traces of (Ca2+)c (left) and (Ca2+)m (right): In UCP2-/- cardiomyocytes rate of rise of (Ca2+)c was significantly decreased while the amplitude of (Ca2+)c was unchanged vs. WT (*p2+)m of UCP2-/- cardiomyocytes were significantly decreased vs. WT (*p2+ transients in WT vs. UCP2-/- cardiomyocytes evoked in the presence of 0.2 μM ryanodine, 0.01 mM thapsigargin and 100 nM Ru360. d) Representative traces of transsarcolemmal (Ca2+)c in WT and UCP2-/-, and e-f) Statistical analysis of amplitude (e) and rate of rise (f): In UCP2-/- transsarcolemmal Ca2+ transient amplitude and rate of rise were significantly down-regulated (*pNCX WT vs. UCP2-/- cardiomyocytes: forward INCX was elicited by 1 s of exposure to 5 mM caffeine using a holding potential of -40 mV. No difference in caffeine induced INCX in WT compared to UCP2-/- was found. h) SR Ca2+ load in WT vs. UCP2-/- calculated via the integral of INCX recordings. No difference in SR Ca2+ load between WT and UCP2-/- was detected.</p

Correlation of stress hormone levels and synaptic plasticity.

<p><b>7A</b>, levels in plasma corticosterone (CORT) were found to be negatively correlated with the outcome in late LTP of the four differentially treated groups (as indexed in the diagrams). CORT levels were positively correlated with persistent LTD of the groups in <b>7B</b>. Each data point combines the individual groups' mean CORT and fEPSP slope value for persistent late LTP/LTD.</p

Results of the pre-study for brain exposure investigation.

<p><b>IV.</b>  =  thermal; <b>III.</b>  =  slightly thermal; <b>II.</b>  =  most likely non-thermal; <b>I.</b>  =  non-thermal.</p><p>*) relating to the double-cone waveguide with only 1 of the 6 exposure places occupied.</p><p>**) Due to the varying results for different depths of the anaesthetical state only the range of the measured temperature elevation is given instead of mean and standard deviation.</p><p>***) determined from measured average initial brain temperature elevation via SAR  =  c (ΔT/Δt)|_t = 0 with c = 3854 J/(kg K) the specific heat capacity of brain tissue.</p