Exposure to 835 MHz radiofrequency electromagnetic field induces autophagy in hippocampus but not in brain stem of mice

2017 ◽  
Vol 34 (1) ◽  
pp. 23-35 ◽  
Author(s):  
Ju Hwan Kim ◽  
Da-Hyeon Yu ◽  
Hyo-Jeong Kim ◽  
Yang Hoon Huh ◽  
Seong-Wan Cho ◽  
...  
Keyword(s):  
Brain Stem ◽  
Mobile Phones ◽  
Hippocampal Neurons ◽  
Brain Regions ◽  
Pcr Analysis ◽  
Limited Information ◽  
The Central Nervous System ◽  
Neuronal Functions ◽  
Adaptation Processes ◽  
The Brain

The exploding popularity of mobile phones and their close proximity to the brain when in use has raised public concern regarding possible adverse effects from exposure to radiofrequency electromagnetic fields (RF-EMF) on the central nervous system. Numerous studies have suggested that RF-EMF emitted by mobile phones can influence neuronal functions in the brain. Currently, there is still very limited information on what biological mechanisms influence neuronal cells of the brain. In the present study, we explored whether autophagy is triggered in the hippocampus or brain stem after RF-EMF exposure. C57BL/6 mice were exposed to 835 MHz RF-EMF with specific absorption rates (SAR) of 4.0 W/kg for 12 weeks; afterward, the hippocampus and brain stem of mice were dissected and analyzed. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis demonstrated that several autophagic genes, which play key roles in autophagy regulation, were significantly upregulated only in the hippocampus and not in the brain stem. Expression levels of LC3B-II protein and p62, crucial autophagic regulatory proteins, were significantly changed only in the hippocampus. In parallel, transmission electron microscopy (TEM) revealed an increase in the number of autophagosomes and autolysosomes in the hippocampal neurons of RF-EMF-exposed mice. The present study revealed that autophagy was induced in the hippocampus, not in the brain stem, in 835 MHz RF-EMF with an SAR of 4.0 W/kg for 12 weeks. These results could suggest that among the various adaptation processes to the RF-EMF exposure environment, autophagic degradation is one possible mechanism in specific brain regions.

Hippocampus is more vulnerable to neural damages induced by repeated sevoflurane exposure in the second trimester than other brain areas

2020 ◽  
Vol 52 (8) ◽  
pp. 864-874
Author(s):  
Bing Chen ◽  
Yanjun Liu ◽  
Yirong Cai ◽  
Dan Tang ◽  
Saihong Xu ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Brain Regions ◽  
Sensitive Period ◽  
Second Trimester ◽  
Brain Areas ◽  
Axon Development ◽  
The Central Nervous System ◽  
New Perspective ◽  
Anesthetic Exposure ◽  
The Brain

Abstract During the rapidly developing and sensitive period of the central nervous system (CNS), a harmful stimulus may have serious consequences. The effect of anesthetic exposure on the development of the offspring’s CNS during pregnancy is still unclear and has been widely concerned. In the present study, we compared the susceptibility of the hippocampus with those of other brain regions in offsprings when the mother mice were exposed to repeated sevoflurane. We found that other than affecting motor sensation, emotion, or social behavior of offspring mice, repeated sevoflurane exposure induced significant memory deficiency. Compared with other brain regions, the hippocampus, which is the key component of the brain serving for learning and memory, was more vulnerable to repeated sevoflurane exposure. We also found that repeated sevoflurane exposure to mother mice could inhibit the axon development of hippocampal neurons. We also predicted that N6-methyladenosine modification of mRNA might play an essential role in the vulnerability of the hippocampus to sevoflurane, while the underlying cellular mechanism needs to be explored in the future. Our study may provide a new perspective for studying the mechanism of hippocampus-specific injury induced by sevoflurane exposure.

Brain stem – from general view to computational model based on switchboard rules of operation

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Włodzisław Duch ◽  
Dariusz Mikołajewski
Keyword(s):  
Brain Stem ◽  
Large Scale ◽  
Ionic Channels ◽  
General View ◽  
The Central Nervous System ◽  
Network States ◽  
Large Scale Simulations ◽  
Influence Of Noise ◽  
The Brain ◽  
Sufficient Precision

Abstract Despite great progress in understanding the functions and structures of the central nervous system (CNS) the brain stem remains one of the least understood systems. We know that the brain stem acts as a decision station preparing the organism to act in a specific way, but such functions are rather difficult to model with sufficient precision to replicate experimental data due to the scarcity of data and complexity of large-scale simulations of brain stem structures. The approach proposed in this article retains some ideas of previous models, and provides more precise computational realization that enables qualitative interpretation of the functions played by different network states. Simulations are aimed primarily at the investigation of general switching mechanisms which may be executed in brain stem neural networks, as far as studying how the aforementioned mechanisms depend on basic neural network features: basic ionic channels, accommodation, and the influence of noise.

NEUROLOGIC DISEASES IN INFANCY AND CHILDHOOD

PEDIATRICS ◽  
1957 ◽  
Vol 19 (5) ◽  
pp. 949-957
Author(s):  
William A. Hawke ◽  
John S. Prichard
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Brain Stem ◽  
Developmental Patterns ◽  
Basic Emotions ◽  
Neurologic Diseases ◽  
Neurologic Disorders ◽  
Infancy And Childhood ◽  
The Central Nervous System ◽  
The Brain

THE SEMINAR was conducted in four 3-hour sessions and aimed to cover the more important features of pediatric neurology. DEVELOPMENT Dr. Hawke reviewed the normal development of the central nervous system in the infant and child which is so important in the assessment of neurologic disorders in this age group. It was noted that the nervous system was particularly immature and changing rapidly in the first 2 years of life. Development was related to myelination and it was emphasized that this was not a steady process but a pattern of sequences of rapid and slow growth. Motor and sensory development appeared to develop from above and to proceed downward, so that eye-control develops before hand- and legcontrol. Development was related to three functioning levels of the central nervous system—the brain stem, the archipallium, and the neopallium. It was observed that the newborn baby functioned at the brain stem level, and to illustrate this an example was given of the hydranencephalic baby which behaves perfectly normally for the first few weeks of life. The anchipallium, which includes part of the temporal lobe, the cingulate gyrus and basal ganglia, supervenes on the brain stem and may be considered responsible for the basic emotions and some primitive motor and sensory control. The neopallium, which includes most of the cerebral hemisphere, becomes dominant in primates. Its function is intellectual rather than emotional and is responsible for skills, discrimination and fine movements. The clinical application of these developmental patterns are innumerable but illustrations were given of changes in physical signs in static brain lesions.

Symptoms, Related Brain Regions, and Diagnosis

2013 ◽  
Author(s):  
J. Eric Ahlskog
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Basal Ganglia ◽  
Brain Stem ◽  
Muscle Activation ◽  
Sensory Information ◽  
Brain Regions ◽  
Electrical Signal ◽  
Brain And Spinal Cord ◽  
The Brain

As a prelude to the treatment chapters that follow, we need to define and describe the types of problems and symptoms encountered in DLB and PDD. The clinical picture can be quite varied: problems encountered by one person may be quite different from those encountered by another person, and symptoms that are problematic in one individual may be minimal in another. In these disorders, the Lewy neurodegenerative process potentially affects certain nervous system regions but spares others. Affected areas include thinking and memory circuits, as well as movement (motor) function and the autonomic nervous system, which regulates primary functions such as bladder, bowel, and blood pressure control. Many other brain regions, by contrast, are spared or minimally involved, such as vision and sensation. The brain and spinal cord constitute the central nervous system. The interface between the brain and spinal cord is by way of the brain stem, as shown in Figure 4.1. Thought, memory, and reasoning are primarily organized in the thick layers of cortex overlying lower brain levels. Volitional movements, such as writing, throwing, or kicking, also emanate from the cortex and integrate with circuits just below, including those in the basal ganglia, shown in Figure 4.2. The basal ganglia includes the striatum, globus pallidus, subthalamic nucleus, and substantia nigra, as illustrated in Figure 4.2. Movement information is integrated and modulated in these basal ganglia nuclei and then transmitted down the brain stem to the spinal cord. At spinal cord levels the correct sequence of muscle activation that has been programmed is accomplished. Activated nerves from appropriate regions of the spinal cord relay the signals to the proper muscles. Sensory information from the periphery (limbs) travels in the opposite direction. How are these signals transmitted? Brain cells called neurons have long, wire-like extensions that interface with other neurons, effectively making up circuits that are slightly similar to computer circuits; this is illustrated in Figure 4.3. At the end of these wire-like extensions are tiny enlargements (terminals) that contain specific biological chemicals called neurotransmitters. Neurotransmitters are released when the electrical signal travels down that neuron to the end of that wire-like process.

scholarly journals Leptin Controls Glutamatergic Synaptogenesis and NMDA-Receptor Trafficking via Fyn Kinase Regulation of NR2B

Endocrinology ◽  
2019 ◽  
Vol 161 (2) ◽  
Author(s):  
Tyler Bland ◽  
Mingyan Zhu ◽  
Crystal Dillon ◽  
Gulcan Semra Sahin ◽  
Jose Luis Rodriguez-Llamas ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Hippocampal Neurons ◽  
Leptin Receptor ◽  
Kinase Inhibitor ◽  
Phosphorylation Site ◽  
Surface Expression ◽  
Brain Regions ◽  
Dominant Negative ◽  
Nmda Receptor Function ◽  
The Central Nervous System

Abstract Activation of the leptin receptor, LepRb, by the adipocytokine/neurotrophic factor leptin in the central nervous system has procognitive and antidepressive effects. Leptin has been shown to increase glutamatergic synaptogenesis in multiple brain regions. In contrast, mice that have a mutation in the LepRb gene show abnormal synapse development in the hippocampus as well as deficits in cognition and increased depressive-like symptoms. Leptin increases glutamatergic synaptogenesis, in part, through enhancement of N-methyl-D-aspartic acid (NMDA) receptor function; yet the underlying signaling pathway is not known. In this study, we examine how leptin regulates surface expression of NR2B-containing NMDA receptors in hippocampal neurons. Leptin stimulation increases NR2BY1472 phosphorylation, which is inhibited by the Src family kinase inhibitor, PP1. Moreover, we show that Fyn, a member of the Src family kinases, is required for leptin-stimulated NR2BY1472 phosphorylation. Furthermore, inhibiting Y1472 phosphorylation with either a dominant negative Fyn mutant or an NR2B mutant that lacks the phosphorylation site (NR2BY1472F) blocks leptin-stimulated synaptogenesis. Additionally, we show that LepRb forms a complex with NR2B and Fyn. Taken together, these findings expand our knowledge of the LepRb interactome and the mechanisms by which leptin stimulates glutamatergic synaptogenesis in the developing hippocampus. Comprehending these mechanisms is key for understanding dendritic spine development and synaptogenesis, alterations of which are associated with many neurological disorders.

scholarly journals Identification of the SNARE complex mediating the exocytosis of NMDA receptors

2016 ◽  
Vol 113 (43) ◽  
pp. 12280-12285 ◽  
Author(s):  
Yi Gu ◽  
Richard L. Huganir
Keyword(s):  
Nmda Receptors ◽  
Hippocampal Neurons ◽  
Total Internal Reflection ◽  
De Novo ◽  
Receptor Trafficking ◽  
Snare Complex ◽  
Synaptic Membranes ◽  
Rab Proteins ◽  
The Central Nervous System ◽  
The Brain

In the central nervous system, NMDA receptors mediate excitatory neurotransmissions and play important roles in synaptic plasticity. The regulation of NMDA receptor trafficking is critical for neural functions in the brain. Here, we directly visualized individual exocytic events of NMDA receptors in rat hippocampal neurons by total internal reflection fluorescence microscopy (TIRFM). We found that the constitutive exocytosis of NMDA receptors included both de novo exocytic and recycling events, which were regulated by different Rab proteins. We also identified the SNAP25–VAMP1–syntaxin4 complex mediating the constitutive exocytosis of NMDA receptors. Transient knockdown of each component of the SNARE complex interfered with surface delivery of NMDA receptors to both extrasynaptic and synaptic membranes. Our study uncovers the postsynaptic function of the SNAP25–VAMP1–syntaxin4 complex in mediating the constitutive exocytosis of NMDA receptors, suggesting that this SNARE complex is involved in excitatory synaptic transmission.

scholarly journals Effects of tiletamine-xylazine-tramadol combination and its specific antagonist on AMPK in the brain of rats

2019 ◽  
Vol 63 (2) ◽  
pp. 285-292
Author(s):  
Ning Ma ◽  
Xin Li ◽  
Hong-bin Wang ◽  
Li Gao ◽  
Jian-hua Xiao
Keyword(s):  
Mrna Expression ◽  
Opposite Effect ◽  
Brain Regions ◽  
Control Group ◽  
Sprague Dawley ◽  
Sd Rats ◽  
The Central Nervous System ◽  
Specific Antagonist ◽  
Sedation And Analgesia ◽  
The Brain

AbstractIntroduction:Tiletamine-xylazine-tramadol (XFM) has few side effects and can provide good sedation and analgesia. Adenosine 5’-monophosphate-activated protein kinase (AMPK) can attenuate trigeminal neuralgia. The study aimed to investigate the effects of XFM and its specific antagonist on AMPK in different regions of the brain.Material and Methods:A model of XFM in the rat was established. A total of 72 Sprague Dawley (SD) rats were randomly divided into three equally sized groups: XFM anaesthesia (M group), antagonist (W group), and XFM with antagonist interactive groups (MW group). Eighteen SD rats were in the control group and were injected intraperitoneally with saline (C group). The rats were sacrificed and the cerebral cortex, cerebellum, hippocampus, thalamus, and brain stem were immediately separated, in order to detect AMPKα mRNA expression by quantitative PCR.Results:XFM was able to increase the mRNA expression of AMPKα1 and AMPKα2 in all brain regions, and the antagonist caused the opposite effect, although the effects of XFM could not be completely reversed in some areas.Conclusion:XFM can influence the expression of AMPK in the central nervous system of the rat, which can provide a reference for the future development of anaesthetics for animals.

scholarly journals Astrocytes, Noradrenaline, α1-Adrenoreceptors, and Neuromodulation: Evidence and Unanswered Questions

2021 ◽  
Vol 15 ◽  
Author(s):  
Jérôme Wahis ◽  
Matthew G. Holt
Keyword(s):  
Critical Appraisal ◽  
Brain Regions ◽  
Synaptic Activity ◽  
Physiological Effects ◽  
Astrocyte Heterogeneity ◽  
Main Effect ◽  
The Central Nervous System ◽  
Noradrenergic Modulation ◽  
The Brain ◽  
Experimental Strategies

Noradrenaline is a major neuromodulator in the central nervous system (CNS). It is released from varicosities on neuronal efferents, which originate principally from the main noradrenergic nuclei of the brain – the locus coeruleus – and spread throughout the parenchyma. Noradrenaline is released in response to various stimuli and has complex physiological effects, in large part due to the wide diversity of noradrenergic receptors expressed in the brain, which trigger diverse signaling pathways. In general, however, its main effect on CNS function appears to be to increase arousal state. Although the effects of noradrenaline have been researched extensively, the majority of studies have assumed that noradrenaline exerts its effects by acting directly on neurons. However, neurons are not the only cells in the CNS expressing noradrenaline receptors. Astrocytes are responsive to a range of neuromodulators – including noradrenaline. In fact, noradrenaline evokes robust calcium transients in astrocytes across brain regions, through activation of α1-adrenoreceptors. Crucially, astrocytes ensheath neurons at synapses and are known to modulate synaptic activity. Hence, astrocytes are in a key position to relay, or amplify, the effects of noradrenaline on neurons, most notably by modulating inhibitory transmission. Based on a critical appraisal of the current literature, we use this review to argue that a better understanding of astrocyte-mediated noradrenaline signaling is therefore essential, if we are ever to fully understand CNS function. We discuss the emerging concept of astrocyte heterogeneity and speculate on how this might impact the noradrenergic modulation of neuronal circuits. Finally, we outline possible experimental strategies to clearly delineate the role(s) of astrocytes in noradrenergic signaling, and neuromodulation in general, highlighting the urgent need for more specific and flexible experimental tools.

scholarly journals The ATF6β-calreticulin axis promotes neuronal survival under endoplasmic reticulum stress and excitotoxicity

2021 ◽  
Author(s):  
Dinh Thi Nguyen ◽  
Thuong Manh Le ◽  
Tsuyoshi Hattori ◽  
Mika Takarada-Iemata ◽  
Hiroshi Ishii ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Hippocampal Neurons ◽  
Neuronal Survival ◽  
Binding Capacity ◽  
Critical Role ◽  
Er Stress Response ◽  
The Central Nervous System ◽  
The Brain

AbstractWhile ATF6α plays a central role in the endoplasmic reticulum (ER) stress response, the function of ATF6β is largely unknown. Here, we demonstrate that ATF6β is highly expressed in the hippocampus of the brain, and specifically regulates the expression of calreticulin, a molecular chaperone in the ER with a high Ca2+-binding capacity. Calreticulin expression was reduced to ~50% in the central nervous system of Atf6b−/− mice, and restored by ATF6β. Analysis using cultured hippocampal neurons revealed that ATF6β deficiency reduced Ca2+ stores in the ER and enhanced ER stress-induced death, which was rescued by ATF6β, calreticulin, Ca2+-modulating reagents such as BAPTA-AM and 2-APB, and ER stress inhibitor salubrinal. In vivo, kainate-induced neuronal death was enhanced in hippocampi of Atf6b−/− and Calr+/− mice, and restored by 2-APB and salubrinal. These results suggest that the ATF6β-calreticulin axis plays a critical role in the neuronal survival by improving Ca2+ homeostasis under ER stress.

scholarly journals Neuromediator systems in some brain regions of rats subjected to morphine intoxication

2010 ◽  
Vol 56 (5) ◽  
pp. 562-569
Author(s):  
S.V. Lelevich ◽  
A.A. Novokshonov
Keyword(s):  
Brain Stem ◽  
Brain Tissue ◽  
Brain Regions ◽  
Cerebral Hemispheres ◽  
Serotonin Level ◽  
Chronic Morphine ◽  
Chronic Morphine Intoxication ◽  
System Functioning ◽  
Gaba Content ◽  
The Brain

The content of neuromediators and its metabolites in the cortex of cerebral hemispheres, in thalamus and brain stem was studied under chronic morphine intoxication (7-21 days). The morphine intake during 7-14 days was accompanied by changes of catecholamine system functioning, which was the most pronounced in the thalamus and the brain stem. These changes included increased secretion of dophamine and noradrenaline, their decrease in the brain tissue, and the increased content of their metabolites. The changes of serotonin and GABA content were less pronounced and included a decrease of serotonin level and the increase of the GABA content in different periods of narcotization.

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