The neuroprotective effects of baobab and black seed on the rat hippocampus exposed to a 900-MHz electromagnetic field.

This study investigated the potential effects on the hippocampus of electromagnetic fields (EMFs) disseminated by mobile phones and the roles of baobab (Adansonia digitata) (AD) and black seed (Nigella sativa) (BS) in mitigating these. Fifty-six male, 12-week-old Wistar albino rats were divided into eight groups of seven animals each. No EMF exposure was applied to the control, AD or BS groups, while the rats in the Sham group were placed in an EMF system with no exposure. A 900-MHz EMF was applied to the EMF+AD, EMF+BS, EMF+AD+BS and EMF groups for 1 hour a day for 28 days. Pyramidal neurons in the hippocampus were subsequently counted using the optical fractionator technique, one of the unbiased stereological methods. Tissue sections were also evaluated histopathologically under light and electron microscopy. The activities of the enzymes catalase (CAT) and superoxide dismutase (SOD) were also determined in blood serum samples. Analysis of the stereological data revealed no statistically significant differences between the EMF and control or sham groups in terms of pyramidal neuron numbers (p>0.05). However, stereological examination revealed a crucial difference in the entire hippocampus between the control group and the AD (p<0.01) and BS (p<0.05) groups. Moreover, exposure to 900-MHz EMF produced adverse changes in the structures of neurons at histopathological analysis. Qualitative examinations suggest that a combination of herbal products such as AD and BS exerts a protective effect against such EMF side-effects.

Photostimulation activates fast-spiking interneurons and pyramidal cells in the entorhinal cortex of Thy1-ChR2-YFP line 18 mice.

The application of optogenetics in animals has provided new insights into both fundamental neuroscience and diseases of the nervous system. This is primarily due to the fact that optogenetics allows selectively activating or inhibiting particular types of neurons. One of the first transgenic mouse lines developed for the optogenetic experiment was Thy1-ChR2-YFP. Thy1 is an immunoglobulin superfamily member expressing in projection neurons, so it was assumed that channelrhodopsin-2 (ChR2) would be primarily expressed in projection neurons. However, the specificity of ChR2 expression under promoter Thy1 in different lines has to be clarified yet. Therefore, we aimed to determine the cell specificity of ChR2 expression in the entorhinal cortex of Thy1-ChR2-YFP line 18 mice. We have found that both pyramidal cells and fast-spiking interneurons in deep layers of the entorhinal cortex depolarized and fired in response to 470-nm photostimulation. To exclude the effect of synaptic activation of interneurons by pyramidal cells, we used a selective antagonist of AMPA receptors. Under these conditions, inhibitory postsynaptic currents decreased but did not disappear completely. Furthermore, gabazine inhibited these postsynaptic currents entirely, thus confirming the direct activation of interneurons by light. These data demonstrate that ChR2 is expressed in both pyramidal neurons and fast-spiking interneurons of the entorhinal cortex in Thy1-ChR2-YFP mice.

Activity labeling in vivo using CaMPARI2 reveals intrinsic and synaptic differences between neurons with high and low firing rate set points.

Neocortical pyramidal neurons regulate firing around a stable mean firing rate (FR) that can differ by orders of magnitude between neurons, but the factors that determine where individual neurons sit within this broad FR distribution are not understood. To access low- and high-FR neurons for ex vivo analysis, we used Ca2+- and UV-dependent photoconversion of CaMPARI2 in vivo to permanently label neurons according to mean FR. CaMPARI2 photoconversion was correlated with immediate early gene expression and higher FRs ex vivo and tracked the drop and rebound in ensemble mean FR induced by prolonged monocular deprivation. High-activity L4 pyramidal neurons had greater intrinsic excitability and recurrent excitatory synaptic strength, while E/I ratio, local output strength, and local connection probability were not different. Thus, in L4 pyramidal neurons (considered a single transcriptional cell type), a broad mean FR distribution is achieved through graded differences in both intrinsic and synaptic properties.

Prenatal and early postnatal exposure to radiofrequency waves (900 MHz) adversely affects passive avoidance learning and memory.

Prenatal and early postnatal are the most sensitive and high-risk periods to expose to electromagnetic fields (EMFs). This study aimed to investigate the effect of prenatal and early postnatal exposure to 900 MHz radiofrequency waves (RFWs) emitted from a base transceiver station antenna on passive avoidance learning and memory (PALM) and hippocampus histomorphology. Female Sprague Dawley rats (190-230 g) were paired with males. The mated rats, confirmed by observing a vaginal plug, were divided into two groups; control and exposed. The control group (n = 7) was not exposed to RFW. The exposed group was divided into three subgroups (n = 8); exposed Ⅰ, exposed during the gestational period (fetal life), and exposed Ⅱ and Ⅲ (postnatal exposure), exposed to RFW during the first 21 days of life, for 2 h/d and 4 h/d, respectively. PALM was evaluated by a shuttle box in 45-day-old pups. Learning and memory of animals were demonstrated as the duration of remaining within the light area, which is called the lighting time. Histological sections were prepared from brain tissues and stained with hematoxylin and eosin. An impairment in the PALM performance was noticed in all exposed subgroups (Ⅰ, Ⅱ, and Ⅲ) (p < 0.05). Learning (short-term memory) and retention (long-term memory) behaviors were more affected in exposed subgroup Ⅰ (prenatal exposed) compared to other postnatal exposed subgroups (Ⅱ and Ⅲ). Also, a mild decrease in the density of pyramidal cells was observed in the hippocampus of exposed subgroups (Ⅰ and Ⅲ). Prenatal and early postnatal exposure to 900 MHz RFW adversely affected PALM performance and hippocampus tissue in rat pups with more impact for prenatal period exposure.

Modulation of Coordinated Activity across Cortical Layers by Plasticity of Inhibitory Synapses.

In the neocortex, synaptic inhibition shapes all forms of spontaneous and sensory evoked activity. Importantly, inhibitory transmission is highly plastic, but the functional role of inhibitory synaptic plasticity is unknown. In the mouse barrel cortex, activation of layer (L) 2/3 pyramidal neurons (PNs) elicits strong feedforward inhibition (FFI) onto L5 PNs. We find that FFI involving parvalbumin (PV)-expressing cells is strongly potentiated by postsynaptic PN burst firing. FFI plasticity modifies the PN excitation-to-inhibition (E/I) ratio, strongly modulates PN gain, and alters information transfer across cortical layers. Moreover, our LTPi-inducing protocol modifies firing of L5 PNs and alters the temporal association of PN spikes to γ-oscillations both in vitro and in vivo. All of these effects are captured by unbalancing the E/I ratio in a feedforward inhibition circuit model. Altogether, our results indicate that activity-dependent modulation of perisomatic inhibitory strength effectively influences the participation of single principal cortical neurons to cognition-relevant network activity.

Spatiotemporal constraints on optogenetic inactivation in cortical circuits.

Optogenetics allows manipulations of genetically and spatially defined neuronal populations with excellent temporal control. However, neurons are coupled with other neurons over multiple length scales, and the effects of localized manipulations thus spread beyond the targeted neurons. We benchmarked several optogenetic methods to inactivate small regions of neocortex. Optogenetic excitation of GABAergic neurons produced more effective inactivation than light-gated ion pumps. Transgenic mice expressing the light-dependent chloride channel GtACR1 produced the most potent inactivation. Generally, inactivation spread substantially beyond the photostimulation light, caused by strong coupling between cortical neurons. Over some range of light intensity, optogenetic excitation of inhibitory neurons reduced activity in these neurons, together with pyramidal neurons, a signature of inhibition-stabilized neural networks ('paradoxical effect'). The offset of optogenetic inactivation was followed by rebound excitation in a light dose-dependent manner, limiting temporal resolution. Our data offer guidance for the design of in vivo optogenetics experiments.

Ultrasound improves the outcomes of cardiopulmonary resuscitation in rats by stimulating the cholinergic anti­inflammatory pathway.

The present study investigated the effects of the ultrasound (US), a noninvasive technique, on ischemia­reperfusion injury (IRI) following cardiopulmonary resuscitation (CPR). The animals used in the present study were randomized into five groups (n=8 per group) as follows: i) The CPR group, where the rats underwent 6 min of untreated ventricular fibrillation (VF) followed by CPR and defibrillation; ii) the US group, in which the treatment was identical to the CPR group with the exception that rats were exposed to US treatment 24 h prior to CPR; iii) the MLA group, in which the treatment was identical to the US group with the exception that the α7 nicotinic acetylcholine receptor (α7nAChR) antagonist MLA (4 mg/kg) was administered 30 min prior to US and VF respectively; iv) the GTS group, in which the treatment was identical to the CPR group with the exception that the α7nAChR agonist GTS­21 (4 mg/kg) was injected 30 min prior to VF; and v) the SHAM group, in which the rats were exposed to surgical preparation without CPR and US application. At 1 day prior to CPR, the US treatment was administered to the left kidney by US pulses (contrast general mode with 9 MHz) with a bursting mechanical index of 0.72 for 2 min. Following treatment of the left kidney, the right kidney was exposed to identical US treatment for an additional 2 min. The results demonstrated that US preconditioning decreased the number of defibrillations required and shortened the duration of CPR. US also suppressed tumor necrosis factor­α and interleukin­6 levels following resuscitation (P<0.05), and a significantly longer overall survival time was observed in the US­treated animals (P<0.01). In addition, US attenuated neuronal injury and promoted the expression of α7nAChR in hippocampal neurons (P<0.05). However, the protective effects of US were abolished by MLA and imitated by GTS­21. The results of the present study demonstrated that prior exposure to US may improve animal outcomes following CPR, and the protective effects of US may be dependent on the cholinergic anti­inflammatory pathway (CAP) via α7nAChR.

Changes in pyramidal and granular neuron numbers in the rat hippocampus 7 days after exposure to a continuous 900-MHz electromagnetic field during early and mid-adolescence.

The aim of this study was to investigate qualitative and quantitative changes in pyramidal and granule neurons in the male rat hippocampus after exposure to a continuous 900-megahertz (MHz) electromagnetic field (EMF) for 25 days during early and mid-adolescence. Three-week-old (21 day) healthy Sprague Dawley male rats were divided equally into control (CON), pseudo-exposed (PEX) and EMF groups. EMF rats were exposed to a 900-MHz EMF in an EMF-application cage, while the PEX rats were placed in the same cage without being exposed to EMF. No procedure was performed in CON. EMF was applied for 1 h/day, every day for 25 days. Following the 900-MHz EMF and pseudo-exposed applications, behavioral tests were performed for seven days. Then, all animals were euthanized and their brains were removed. Following histological tissue procedures, sections were taken from tissues and stained with toluidine blue. The optical fractionation technique was performed to estimate the pyramidal neuron numbers in the CA1, CA2-3 and hilus regions of the hippocampus and granule neuron numbers in the dentate gyrus region. Our findings indicated that the number of pyramidal and granule neurons in the hippocampus of the EMF group was statistically higher than PEX. Furthermore, the histopathological results showed that the cytoplasm of pyramidal (in the hilus, CA1, CA2 and CA3 region) and granular (in the dentate gyrus region) cells at the hippocampus were disrupted, as evident by intensive staining around cytoplasm and some artifacts were detected in the EMF group. In addition, statistical comparisons of the mean body weights and brain weights of the study groups revealed no significant differences. There was no statistically significant difference between the PEX and EMF groups in terms of temperature (p > 0.05) or humidity (p > 0.05) in the cages. In conclusion, higher numbers of both pyramidal and granule neurons were found in the male rat hippocampus after continuous 900-MHz EMF treatment.

Multi-site dynamic recording for Aß oligomers-induced Alzheimer's disease in vitro based on neuronal network chip.

Alzheimer's disease (AD) is a chronic central neurodegenerative disease. The pathological features of AD are the extracellular deposition of senile plaques formed by amyloid-ß oligomers (AßOs) and the intracellular accumulation of neurofibrillary tangles. However, due to the lack of effective method and experimental models to study the cognitive decline, communication at cell resolution and the implementation of interventions, the diagnosis and treatment on AD still progress slowly. In this paper, we established a pathological model of AD in vitro based on AßOs-induced hippocampal neuronal network chip for multi-site dynamic analysis of the neuronal electrical activity and network connection. The multiple characteristic parameters, including positive and negative spike intervals, firing rate and peak-to-peak values, were extracted through the analysis of spike signals, and two firing patterns from the interneurons and pyramidal neurons were recorded. The spatial firing patterns mapping and cross-correlation between channels were performed to validate the degeneration of neuronal network connectivity. Moreover, an electrical stimulation with frequency at 40 Hz was exerted to preliminarily explore the therapeutic effect on the pathological model of AD. This neuronal network chip enables the implementation of AD models in vitro for studying basic mechanisms of neurodegeneration within networks and for the parallel testing of various potential therapies. It can be a novel technique in the research of AD pathological model in vitro.

Whole-Body 12C Irradiation Transiently Decreases Mouse Hippocampal Dentate Gyrus Proliferation and Immature Neuron Number, but Does Not Change New Neuron Survival Rate.

High-charge and -energy (HZE) particles comprise space radiation and they pose a challenge to astronauts on deep space missions. While exposure to most HZE particles decreases neurogenesis in the hippocampus-a brain structure important in memory-prior work suggests that 12C does not. However, much about 12C's influence on neurogenesis remains unknown, including the time course of its impact on neurogenesis. To address this knowledge gap, male mice (9⁻11 weeks of age) were exposed to whole-body 12C irradiation 100 cGy (IRR; 1000 MeV/n; 8 kEV/µm) or Sham treatment. To birthdate dividing cells, mice received BrdU i.p. 22 h post-irradiation and brains were harvested 2 h (Short-Term) or three months (Long-Term) later for stereological analysis indices of dentate gyrus neurogenesis. For the Short-Term time point, IRR mice had fewer Ki67, BrdU, and doublecortin (DCX) immunoreactive (+) cells versus Sham mice, indicating decreased proliferation (Ki67, BrdU) and immature neurons (DCX). For the Long-Term time point, IRR and Sham mice had similar Ki67+ and DCX+ cell numbers, suggesting restoration of proliferation and immature neurons 3 months post-12C irradiation. IRR mice had fewer surviving BrdU+ cells versus Sham mice, suggesting decreased cell survival, but there was no difference in BrdU+ cell survival rate when compared within treatment and across time point. These data underscore the ability of neurogenesis in the mouse brain to recover from the detrimental effect of 12C exposure.

Postnatal development of inhibitory synaptic transmission in the anterior piriform cortex.

The morphological and functional development of inhibitory circuit in the anterior piriform cortex (aPC) during the first three postnatal weeks may be crucial for the development of odor preference learning in infant rodents. As first step toward testing this hypothesis, we examined the normal development of GABAergic synaptic transmission in the aPC of rat pups during the postnatal days (P) 5-8 and 14-17. Whole cell patch-clamp recordings of layer 2/3 (L2/3) aPC pyramidal cells revealed a significant increase in spontaneous (sIPSC) and miniature (mIPSC) inhibitory postsynaptic current frequencies and a decrease in mIPSC rise and decay-time constant at P14-P17. Moreover, as the development of neocortical inhibitory circuit can be driven by sensory experience, we recorded sIPSC and mIPSC onto L2/3 aPC pyramidal cells from unilateral naris-occluded animals. Early partial olfactory deprivation caused by naris occlusion do not affected the course of age-dependent increase IPSC frequency onto L2/3 aPC pyramidal cell. However, this age-dependent increase of sIPSC and mIPSC frequencies were lower on aPC pyramidal cells ipsilateral to the occlusion side. In addition, the age-dependent increase in sIPSC frequency and amplitude were more pronounced on aPC pyramidal cells contralateral to the occlusion. While mIPSC kinetics were not affected by age or olfactory deprivation, at P5-P8, the sIPSC decay-time constant on aPC pyramidal cells of both hemispheres of naris-occluded animals were significantly higher when compared to sham. These results demonstrated that the GABAergic synaptic transmission on the aPC changed during postnatal development by increasing inhibitory inputs on L2/3 pyramidal cells, with increment in frequency of both sIPSC and mIPSC and faster kinetics of mIPSC. Our data suggested that the maturation of GABAergic synaptic transmission was little affected by early partial olfactory deprivation. These results could contribute to unravel the mechanisms underlying the development of odor processing and olfactory preference learning.

Histopathological, immunohistochemical, and stereological analysis of the effect of Ginkgo biloba (Egb761) on the hippocampus of rats exposed to long-term cellphone radiation.

Cellular phones are major sources of electromagnetic radiation (EMR) that can penetrate the human body and pose serious health hazards. The increasingly widespread use of mobile communication systems has raised concerns about the effects of cellphone radiofrequency (RF) on the hippocampus because of its close proximity to radiation during cellphone use. The effects of cellphone EMR exposure on the hippocampus of rats and the possible counteractive effects of Ginkgo biloba (Egb761) were aimed to investigate. Rats were divided into three groups: Control, EMR, and EMR+Egb761. The EMR and EMR+Egb761 groups were exposed to cellphone EMR for one month. Egb761 was also administered to the EMR+Egb761 group. Specifically, we evaluated the effect of RF exposure on rat hippocampi at harmful EMR levels (0.96 W/kg specific absorption rate [SAR]) for one month and also investigated the possible impact of Ginkgo biloba (Egb761) using stereological, TUNEL-staining, and immunohistochemical methods. An increase in apoptotic proteins (Bax, Acas-3) and a decrease in anti-apoptotic protein (Bcl-2) immunoreactivity along with a decrease in the total granule and pyramidal cell count were noted in the EMR group. A decrease in Bax and Acas-3 and an increase in Bcl-2 immunoreactivity were observed in rats treated with Egb761 in addition to a decrease in TUNEL-stained apoptotic cells and a higher total viable cell number. In conclusion, chronic cellphone EMR exposure may affect hippocampal cell viability, and Egb761 may be used to mitigate some of the deleterious effects.

Effect of 1.8 GHz radiofrequency electromagnetic radiation on novel object associative recognition memory in mice.

Mounting evidence suggests that exposure to radiofrequency electromagnetic radiation (RF-EMR) can influence learning and memory in rodents. In this study, we examined the effects of single exposure to 1.8 GHz RF-EMR for 30 min on subsequent recognition memory in mice, using the novel object recognition task (NORT). RF-EMR exposure at an intensity of >2.2 W/kg specific absorption rate (SAR) power density induced a significant density-dependent increase in NORT index with no corresponding changes in spontaneous locomotor activity. RF-EMR exposure increased dendritic-spine density and length in hippocampal and prefrontal cortical neurons, as shown by Golgi staining. Whole-cell recordings in acute hippocampal and medial prefrontal cortical slices showed that RF-EMR exposure significantly altered the resting membrane potential and action potential frequency, and reduced the action potential half-width, threshold, and onset delay in pyramidal neurons. These results demonstrate that exposure to 1.8 GHz RF-EMR for 30 min can significantly increase recognition memory in mice, and can change dendritic-spine morphology and neuronal excitability in the hippocampus and prefrontal cortex. The SAR in this study (3.3 W/kg) was outside the range encountered in normal daily life, and its relevance as a potential therapeutic approach for disorders associated with recognition memory deficits remains to be clarified.

Chloride conducting light activated channel GtACR2 can produce both cessation of firing and generation of action potentials in cortical neurons in response to light.

Optogenetics is a powerful technique in neuroscience that provided a great success in studying the brain functions during the last decade. Progress of optogenetics crucially depends on development of new molecular tools. Light-activated cation-conducting channelrhodopsin2 was widely used for excitation of cells since the emergence of optogenetics. In 2015 a family of natural light activated chloride channels GtACR was identified which appeared to be a very promising tool for using in optogenetics experiments as a cell silencer. Here we examined properties of GtACR2 channel expressed in the rat layer 2/3 pyramidal neurons by means of in utero electroporation. We have found that despite strong inhibition the light stimulation of GtACR2-positive neurons can surprisingly lead to generation of action potentials, presumably initiated in the axonal terminals. Thus, when using the GtACR2 in optogenetics experiments, its ability to induce action potentials should be taken into account. Our results also open an interesting possibility of using the GtACR2 both as cell silencer and cell activator in the same experiment varying the pattern of light stimulation.

Effects of 15 Hz square wave magnetic fields on the voltage-gated sodium and potassium channels in prefrontal cortex pyramidal neurons.

PURPOSE: Although magnetic fields have significant effects on neurons, little is known about the mechanisms behind their effects. The present study aimed to measure the effects of magnetic fields on ion channels in cortical pyramidal neurons. MATERIALS AND METHODS: Cortical pyramidal neurons of Kunming mice were isolated and then subjected to 15 Hz, 1 mT square wave (duty ratio 50%) magnetic fields stimulation. Sodium currents (INa), transient potassium currents (IA) and delayed rectifier potassium currents (IK) were recorded by whole-cell patch clamp method. RESULTS: We found that magnetic field exposure depressed channel current densities, and altered the activation kinetics of sodium and potassium channels. The inactivation properties of INa and IA were also altered. CONCLUSION: Magnetic field exposure alters ion channel function in neurons. It is likely that the structures of sodium and potassium channels were influenced by the applied field. Sialic acid, which is an important component of the channels, could be the molecule responsible for the reported results.

Enhanced Control of Cortical Pyramidal Neurons With Micromagnetic Stimulation.

Magnetic stimulation is less sensitive to the inflammatory reactions that plague conventional electrode-based cortical implants and therefore may be useful as a next-generation (implanted) cortical prosthetic. The fields arising from micro-coils are quite small however and thus, their ability to modulate cortical activity must first be established. Here, we show that layer V pyramidal neurons (PNs) can be strongly activated by micro-coil stimulation and further, the asymmetric fields arising from such coils do not simultaneously activate horizontally-oriented axon fibers, thus confining activation to a focal region around the coil. The spatially-narrow fields from micro-coils allowed the sensitivity of different regions within a single PN to be compared: while the proximal axon was most sensitive in naïve cells, repetitive stimulation over the apical dendrite led to a change in state of the neuron that reduced thresholds there to below those of the axon. Thus, our results raise the possibility that regardless of the mode of stimulation, penetration depths that target specific portions of the apical dendrite may actually be more effective than those that target Layer 6. Interestingly, the state change had similar properties to state changes described previously at the systems level, suggesting a possible neuronal mechanism underlying such responses.

Ncm, a Photolabile Group for Preparation of Caged Molecules: Synthesis and Biological Application.

Ncm, 6-nitrocoumarin-7-ylmethyl, is a photolabile protective group useful for making "caged" molecules. Ncm marries the reliable photochemistry of 2-nitrobenzyl systems with the excellent stability and spectroscopic properties of the coumarin chromophore. From simple, commercially available starting materials, preparation of Ncm and its caged derivatives is both quick and easy. Photorelease of Ncm-caged molecules occurs on the microsecond time scale, with quantum efficiencies of 0.05-0.08. We report the synthesis and physical properties of Ncm and its caged derivatives. The utility of Ncm-caged glutamate for neuronal photostimulation is demonstrated in cultured hippocampal neurons and in brain slice preparations.

Pernicious effects of long-term, continuous 900-MHz electromagnetic field throughout adolescence on hippocampus morphology, biochemistry and pyramidal neuron numbers in 60-day-old Sprague Dawley male rats.

The central nervous system (CNS) begins developing in the intrauterine period, a process that continues until adulthood. Contact with chemical substances, drugs or environmental agents such as electromagnetic field (EMF) during adolescence therefore has the potential to disturb the development of the morphological architecture of components of the CNS (such as the hippocampus). The hippocampus is essential to such diverse functions as memory acquisition and integration and spatial maneuvering. EMF can result in severe damage to both the morphology of the hippocampus and its principal functions during adolescence. Although children and adolescents undergo greater exposure to EMF than adults, the information currently available regarding the effects of exposure to EMF during this period is as yet insufficient. This study investigated the 60-day-old male rat hippocampus following exposure to 900 megahertz (MHz) EMF throughout the adolescent period using stereological, histopathological and biochemical analysis techniques. Eighteen male Sprague Dawley rats aged 21days were assigned into control, sham and EMF groups on a random basis. No procedure was performed on the control group rats. The EMF group (EMFGr) was exposed to a 900-MHz EMF for 1h daily from beginning to end of adolescence. The sham group rats were held in the EMF cage but were not exposed to EMF. All rats were sacrificed at 60days of age. Their brains were extracted and halved. The left hemispheres were set aside for biochemical analyses and the right hemispheres were subjected to stereological and histopathological evaluation. Histopathological examination revealed increased numbers of pyknotic neurons with black or dark blue cytoplasm on EMFGr slides stained with cresyl violet. Stereological analyses revealed fewer pyramidal neurons in EMFGr than in the other two groups. Biochemical analyses showed an increase in malondialdehyde and glutathione levels, but a decrease in catalase levels in EMFGr. Our results indicate that oxidative stress-related morphological damage and pyramidal neuron loss may be observed in the rat hippocampus following exposure to 900-MHz EMF throughout the adolescent period.

Transcranial magnetic stimulation (TMS) inhibits cortical dendrites.

One of the leading approaches to non-invasively treat a variety of brain disorders is transcranial magnetic stimulation (TMS). However, despite its clinical prevalence, very little is known about the action of TMS at the cellular level let alone what effect it might have at the subcellular level (e.g. dendrites). Here, we examine the effect of single-pulse TMS on dendritic activity in layer 5 pyramidal neurons of the somatosensory cortex using an optical fiber imaging approach. We find that TMS causes GABAB-mediated inhibition of sensory-evoked dendritic Ca(2+) activity. We conclude that TMS directly activates fibers within the upper cortical layers that leads to the activation of dendrite-targeting inhibitory neurons which in turn suppress dendritic Ca(2+) activity. This result implies a specificity of TMS at the dendritic level that could in principle be exploited for investigating these structures non-invasively.

Deleterious impacts of a 900-MHz electromagnetic field on hippocampal pyramidal neurons of 8-week-old Sprague Dawley male rats.

Children are at potential risk due to their intense use of mobile phones. We examined 8-week-old rats because this age of the rats is comparable with the preadolescent period in humans. The number of pyramidal neurons in the cornu ammonis of the Sprague Dawley male rat (8-weeks old, weighing 180-250 g) hippocampus following exposure to a 900 MHz (MHz) electromagnetic field (EMF) were examined. The study consisted of control (CN-G), sham exposed (SHM-EG) and EMF exposed (EMF-EG) groups with 6 rats in each. The EMF-EG rats were exposed to 900 MHz EMF (1h/day for 30 days) in an EMF jar. The SHM-EG rats were placed in the EMF jar but not exposed to the EMF (1h/day for 30 days). The CN-G rats were not placed into the exposure jar and were not exposed to the EMF during the study period. All animals were sacrificed at the end of the experiment, and their brains were removed for histopathological and stereological analysis. The number of pyramidal neurons in the cornu ammonis of the hippocampus was estimated on Cresyl violet stained sections of the brain using the optical dissector counting technique. Histopathological evaluations were also performed on these sections. Histopathological observation showed abundant cells with abnormal, black or dark blue cytoplasm and shrunken morphology among the normal pyramidal neurons. The largest lateral ventricles were observed in the EMF-EG sections compared to those from the other groups. Stereological analyses showed that the total number of pyramidal neurons in the cornu ammonis of the EMF-EG rats was significantly lower than those in the CN-G (p<0.05) and the SHM-EG (p<0.05). In conclusion, our results suggest that pyramidal neuron loss and histopathological changes in the cornu ammonis of 8-week-old male rats may be due to the 900-MHz EMF exposure.