Neurophysiological Effects Induced in the Nervous Tissue by Low-Frequency, Pulsed Magnetic Fields

Summary The influence of pulsed magnetic fields (PMF) on the properties of nervous tissue was investigated. Hippocampal slices or synaptosomes obtained from hippocampal tissue were used as model systems. The amplitude of potentials recorded in vitro from one of the hippocampal pathways (Schaffer collaterals that use glutamate as a neurotransmitter) was employed as a measure of the influence of magnetic fields on synaptic efficiency. The synaptic glutamate turnover and radioactive calcium accumulation were used as markers of the PMF influence on biochemistry of synaptic mechanisms. The exposure of hippocampal slices for 30 min to PMF amplified evoked potentials. While the frequency of 0.16 Hz exerted the strongest effect, lower (0.01, 0.07, 0.03 Hz) and higher (0.5 Hz) frequencies were much less effective. The enhancement of the neuronal excitability was correlated with significant increase in the neuronal spontaneous activity mediated by electrical synapses. The PMF-induced changes in the excitability of the tissue were accompanied by an increase in the synaptic turnover of glutamate. The release of radioactive D-Aspartate (a glutamate analog used as a marker for glutamate turnover) from the slices, and its uptake by synaptosomes were enhanced, and reduced respectively, following the stimulation with pulsed magnetic fields. The frequency which was the most efficient in amplification of evoked potentials (0.16 Hz) was also the most effective in the modulation of the release and uptake processes. The PMF-induced changes in neurotransmitter turnover coincided with an increase in ⁴⁵Ca²⁺ accumulation observed in hippocampal slices exposed to PMF.     

50 Hz alternating extremely low frequency magnetic fields affect excitability,firing and action potential shape through interaction with ionic channels in snail neurones

In spite of growing concern about the influence of magnetic fields on biological systems, the interaction between extremely low frequency magnetic field (ELF magnetic fields) and biological structures at the cellular level remains obscure. The aim of this study was to investigate if 50 Hz magnetic fields could have an effect on the neuronal excitability and firing responses. Under Current-Clamp condition, exposure to 50 Hz ELF magnetic fields at 2 mT or 0.8 mT intensities resulted in an increase in the peak amplitude of action potential and after hyperpolaization potential in a time dependent manner. Both magnetic field intensities decreased also the firing frequency and the duration of action potential. Taken together, these data suggest that 50 Hz ELF magnetic fields at 2 mT or 0.8 mT intensities may change the electrophysiological behavior of neuronal cells and underlying ion channel currents.     

Inhibition of rhythmic neural spiking by noise: the occurrence of a minimum in activity with increasing noise

The effects of noise on neuronal dynamical systems are of much current interest. Here, we investigate noise-induced changes in the rhythmic firing activity of single Hodgkin–Huxley neurons. With additive input current, there is, in the absence of noise, a critical mean value μ = μ _c above which sustained periodic firing occurs. With initial conditions as resting values, for a range of values of the mean μ near the critical value, we have found that the firing rate is greatly reduced by noise, even of quite small amplitudes. Furthermore, the firing rate may undergo a pronounced minimum as the noise increases. This behavior has the opposite character to stochastic resonance and coherence resonance. We found that these phenomena occurred even when the initial conditions were chosen randomly or when the noise was switched on at a random time, indicating the robustness of the results. We also examined the effects of conductance-based noise on Hodgkin–Huxley neurons and obtained similar results, leading to the conclusion that the phenomena occur across a wide range of neuronal dynamical systems. Further, these phenomena will occur in diverse applications where a stable limit cycle coexists with a stable focus.     

Social experience influences the development of a central auditory area

Vocal communication develops under social influences that can enhance attention, an important factor in memory formation and perceptual tuning. In songbirds, social conditions can delay sensitive periods of development, overcome learning inhibitions and enable exceptional learning or induce selective learning. However, we do not know how social conditions influence auditory processing in the brain. In the present study, we raised young naive starlings under different social conditions but with the same auditory experience of adult songs, and we compared the effects of these different conditions on the development of the auditory cortex analogue. Several features appeared to be influenced by the social experience, among which the proportion of auditory neuronal sites and the neuronal selectivity. Both physical and social isolation from adult models altered the development of the auditory area in parallel to alterations in vocal development. To our knowledge, this is the first evidence that social deprivation has as much influence on neuronal responsiveness as sensory deprivation.     

Probable exclusion of juvenile neuronal ceroid lipofuscinosis in a fetus at risk: An interim report

In a family with two children affected by juvenile neuronal ceroid lipofuscinosis (JNCL) an attempt was made at the prenatal diagnosis of the disorder. The following tissues from the fetus at risk were investigated by electron microscopy and were found to be free of fingerprint profiles and curvilinear bodies, typical for JNCL: uncultivated amniotic fluid cells, lymphocytes isolated from fetal blood, and fetal skin biopsy specimens. The child was born at the 34th week of gestation and was clinically normal at the age of 15 months. Postnatally, lymphocytes (isolated at the age of 6 and 15 months) and skin tissue (taken at the age of 15 months) were found to be morphologically normal. It is highly unlikely that the child is affected but definite proof of the absence of JNCL remains difficult at this age.     

Particulate matter (PM2.5) exposure season-dependently induces neuronal apoptosis and synaptic injuries

Epidemiological studies have shown that particulate matter 2.5 (PM_2.5) not only increases the incidence of cardiopulmonary illnesses but also relates to the development of neurodegenerative diseases. Considering that PM_2.5 is highly heterogeneous with regional disparity and seasonal variation, we investigated whether PM_2.5 exposure induced neuronal apoptosis and synaptic injuries in a season-dependent manner. The results indicated that PM_2.5 altered the expression of apoptosis-related proteins (mainly bax and bcl-2), activated caspase-3 and caused neuronal apoptosis. Additionally, PM_2.5 decreased the levels of synaptic structural protein postsynaptic density (PSD-95) and synaptic functional protein N-methyl-D-aspartate (NMDA) receptor subunit (NR2B) expression. These effects occurred in a season-dependent manner, and PM_2.5 collected from the winter showed the strongest changes. Furthermore, the effect was coupled with the inhibition of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and phosphorylated cAMP-response element binding protein (p-CREB). Based on the findings, we analyzed the correlations between the chemical composition of PM_2.5 samples and the biological effects, and confirmed that winter PM_2.5 played a major role in causing neuronal apoptosis and synaptic injuries among different season samples.     

Prenatal diagnosis and investigation of a fetus with chondrodysplasia punctata,ichthyosis, and Kallmann syndrome due to an Xp deletion

We report the prenatal diagnosis of a male fetus with X-linked recessive chondrodysplasia punctata (CDPX), steroid sulphatase (STS) deficiency, X-linked Kallmann syndrome (KAL), and a chromosome deletion at Xp22.31. Biochemical analysis of bone from this case indicates that CDPX is not a defect of vitamin K metabolism. Immunocytochemical study of the brain suggests that KAL is a defect in neuronal migration.