scholarly journals Exposure to 2.45 GHz Radiation Triggers Changes in HSP-70, Glucocorticoid Receptors and GFAP Biomarkers in Rat Brain

2021 ◽  
Vol 22 (10) ◽  
pp. 5103
Author(s):  
Haifa Othman ◽  
Alberto López-Furelos ◽  
José Manuel Leiro-Vidal ◽  
Mohamed Ammari ◽  
Mohsen Sakly ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Glucocorticoid Receptors ◽  
Brain Regions ◽  
Repeated Exposure ◽  
Limbic Cortex ◽  
Sprague Dawley ◽  
Hsp 70 ◽  
Tissue Heating ◽  
Radiation Regime ◽  
Set Up

Brain tissue may be especially sensitive to electromagnetic phenomena provoking signs of neural stress in cerebral activity. Fifty-four adult female Sprague-Dawley rats underwent ELISA and immunohistochemistry testing of four relevant anatomical areas of the cerebrum to measure biomarkers indicating induction of heat shock protein 70 (HSP-70), glucocorticoid receptors (GCR) or glial fibrillary acidic protein (GFAP) after single or repeated exposure to 2.45 GHz radiation in the experimental set-up. Neither radiation regime caused tissue heating, so thermal effects can be ruled out. A progressive decrease in GCR and HSP-70 was observed after acute or repeated irradiation in the somatosensory cortex, hypothalamus and hippocampus. In the limbic cortex; however, values for both biomarkers were significantly higher after repeated exposure to irradiation when compared to control animals. GFAP values in brain tissue after irradiation were not significantly different or were even lower than those of nonirradiated animals in all brain regions studied. Our results suggest that repeated exposure to 2.45 GHz elicited GCR/HSP-70 dysregulation in the brain, triggering a state of stress that could decrease tissue anti-inflammatory action without favoring glial proliferation and make the nervous system more vulnerable.

scholarly journals Activity-regulated cytoskeleton-associated protein (Arc/Arg3.1)-mediated plasticity in the paraventricular thalamic nucleus promotes a fundamental adaptation to stress

2021 ◽  
Author(s):  
Brian F Corbett ◽  
Sandra Luz ◽  
Jay Arner ◽  
Abigail Vigderman ◽  
Kimberly Urban ◽  
...  
Keyword(s):  
Neural Activity ◽  
Molecular Mechanisms ◽  
Thalamic Nucleus ◽  
Field Potential ◽  
Brain Regions ◽  
Repeated Exposure ◽  
Designer Drugs ◽  
Sprague Dawley ◽  
Post Traumatic Stress ◽  
Neural Connections

BACKGROUND: Habituation is defined as a progressive decline in response to repeated exposure to a familiar and predictable stimulus and is highly conserved across species. Disrupted habituation is a signature of post-traumatic stress disorder (PTSD). In rodents, habituation is observed in neural, neuroendocrine and behavioral responses to repeated exposure to the predictable and moderately intense stress or restraint. We previously demonstrated that lesions to the posterior division of the paraventricular thalamic nucleus (pPVT) impairs habituation. However, the underlying molecular mechanisms and specific neural connections among the pPVT and other brain regions that underlie habituation are unknown. METHODS: Behavioral and neuroendocrine habituation was assessed in adult male Sprague-Dawley restraints using the repeated restraint paradigm. Pan neuronal and Cre-dependent Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) were used to chemogenetically inhibit the pPVT and the subpopulation of pPVT neurons that project to the medial prefrontal cortex (mPFC), respectively. Activity-regulated cytoskeleton-associated protein (Arc) expression was knocked down in the pPVT using siRNA directed towards Arc. Golgi staining was used to assess structural plasticity of pPVT neurons. Local field potential recordings were used to assess coherent neural activity between the pPVT and mPFC. The attentional set-shifting task was used to assess mPFC-dependent behavior. RESULTS: Here, we show that Arc promotes habituation by increasing stress-induced spinogenesis in the pPVT, increasing coherent neural activity with the mPFC, and improving mPFC-mediated cognitive flexibility. CONCLUSION: Our results demonstrate that Arc induction in the pPVT regulates habituation to repeated restraint and mPFC function.

scholarly journals EEG-based diagnostics of the auditory system using cochlear implant electrodes as sensors

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ben Somers ◽  
Christopher J. Long ◽  
Tom Francart
Keyword(s):  
Cochlear Implant ◽  
Auditory Evoked Potentials ◽  
Human Subjects ◽  
Electrode Array ◽  
Brain Regions ◽  
Hearing Impaired ◽  
Brain Responses ◽  
Listening Environments ◽  
Set Up ◽  
Neural Feedback

AbstractThe cochlear implant is one of the most successful medical prostheses, allowing deaf and severely hearing-impaired persons to hear again by electrically stimulating the auditory nerve. A trained audiologist adjusts the stimulation settings for good speech understanding, known as “fitting” the implant. This process is based on subjective feedback from the user, making it time-consuming and challenging, especially in paediatric or communication-impaired populations. Furthermore, fittings only happen during infrequent sessions at a clinic, and therefore cannot take into account variable factors that affect the user’s hearing, such as physiological changes and different listening environments. Objective audiometry, in which brain responses evoked by auditory stimulation are collected and analysed, removes the need for active patient participation. However, recording of brain responses still requires expensive equipment that is cumbersome to use. An elegant solution is to record the neural signals using the implant itself. We demonstrate for the first time the recording of continuous electroencephalographic (EEG) signals from the implanted intracochlear electrode array in human subjects, using auditory evoked potentials originating from different brain regions. This was done using a temporary recording set-up with a percutaneous connector used for research purposes. Furthermore, we show that the response morphologies and amplitudes depend crucially on the recording electrode configuration. The integration of an EEG system into cochlear implants paves the way towards chronic neuro-monitoring of hearing-impaired patients in their everyday environment, and neuro-steered hearing prostheses, which can autonomously adjust their output based on neural feedback.

scholarly journals miR-142 downregulation alleviates rat PTSD-like behaviors, reduces the level of inflammatory cytokine expression and apoptosis in hippocampus, and upregulates the expression of fragile X mental retardation protein

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Peng-Yin Nie ◽  
Lei Tong ◽  
Ming-Da Li ◽  
Chang-Hai Fu ◽  
Jun-Bo Peng ◽  
...  
Keyword(s):  
Fragile X ◽  
Brain Regions ◽  
Synaptic Proteins ◽  
Sprague Dawley ◽  
Post Traumatic Stress ◽  
Proinflammatory Mediators ◽  
Upstream Regulator ◽  
Trace Fear ◽  
Factor Α

Abstract Background FMRP is a selective mRNA-binding protein that regulates protein synthesis at synapses, and its loss may lead to the impairment of trace fear memory. Previously, we found that FMRP levels in the hippocampus of rats with post-traumatic stress disorder (PTSD) were decreased. However, the mechanism underlying these changes remains unclear. Methods Forty-eight male Sprague-Dawley rats were randomly divided into four groups. The experimental groups were treated with the single-prolonged stress (SPS) procedure and injected with a lentivirus-mediated inhibitor of miR-142-5p. Behavior test as well as morphology and molecular biology experiments were performed to detect the effect of miR-142 downregulation on PTSD, which was further verified by in vitro experiments. Results We found that silence of miRNA-142 (miR-142), an upstream regulator of FMRP, could alleviate PTSD-like behaviors of rats exposed to the SPS paradigm. MiR-142 silence not only decreased the levels of proinflammatory mediators, such as interleukin-1β, interleukin-6, and tumor necrosis factor-α, but also increased the expressive levels of synaptic proteins including PSD95 and synapsin I in the hippocampus, which was one of the key brain regions associated with PTSD. We further detected that miR-142 silence also downregulated the transportation of nuclear factor kappa-B (NF-κB) into the nuclei of neurons and might further affect the morphology of neurons. Conclusions The results revealed miR-142 downregulation could alleviate PTSD-like behaviors through attenuating neuroinflammation in the hippocampus of SPS rats by binding to FMRP.

Enzymatic condensation of dopamine and acetaldehyde: a salsolinol synthase from rat brain

Biologia ◽  
2011 ◽  
Vol 66 (6) ◽  
Author(s):  
Xuechai Chen ◽  
Abida Arshad ◽  
Hong Qing ◽  
Rui Wang ◽  
Jianqing Lu ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Substantia Nigra ◽  
Human Subjects ◽  
Enzymatic Reaction ◽  
Brain Regions ◽  
Activity Detection ◽  
Reaction Products ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Salsolinol Synthase

AbstractSalsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; Sal) is structurally similar to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, which is supposed to have a role in the development of Parkinson-like syndrome in both human and non-human subjects. In the human brain, the amount of (R)-enantiomer of Sal is much higher than (S)-enantiomer, suggesting that a putative enzyme may participate in the synthesis of (R)-salsolinol, called (R)-salsolinol synthase. In this study, the (R)-salsolinol synthase activity in the condensation of dopamine and acetaldehyde was investigated in the crude extracts from the brains of Sprague Dawley rats. Identification of the enzymatic reaction products and enzyme activity detection were achieved by HPLC-electrochemical detection. The discovery of this enzyme activity in rat’s brain indicates the natural existence of (R)-salsolinol synthase in the brains of humans and rats, and it is distributed in most brain regions of rat with higher activity in soluble proteins extracted from striatum and substantia nigra.

Refining the Effects Observed in a Developmental Neurobehavioral Study of Ammonium Perchlorate Administered Orally in Drinking Water to Rats. II. Behavioral and Neurodevelopment Effects

2005 ◽  
Vol 24 (6) ◽  
pp. 451-467 ◽  
Author(s):  
Raymond G. York ◽  
John Barnett ◽  
Michael F. Girard ◽  
David R. Mattie ◽  
Marni V. K. Bekkedal ◽  
...  
Keyword(s):  
Drinking Water ◽  
Ammonium Perchlorate ◽  
Brain Regions ◽  
Male Rats ◽  
Male Rat ◽  
Sprague Dawley ◽  
Continuous Access ◽  
Brain Morphometry ◽  
The Central Nervous System ◽  
The Right

A developmental neurotoxicity study was conducted to generate additional data on the potential functional and morphological hazard to the central nervous system caused by ammonium perchlorate in offspring from in utero and lactation exposure. Female Sprague-Dawley rats (23 to 25/group) were given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 10.0 mg/kg-day perchlorate in the drinking water beginning 2 weeks prior to mating and continuing through day 10 of lactation for the behavioral function assessment or given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 30.0 mg/kg-day beginning on gestation day 0 and continuing through day 10 of lactation for neurodevelopment assessments. Motor activity was conducted on postpartum days 14, 18, and 22 and juvenile brain weights, neurohistopathological examinations, and regional brain morphometry were conducted on postpartum days 10 and 22. This research revealed a sexually dimorphic response, with some brain regions being larger in perchlorate-treated male rats than in comparable controls. Even so, there was no evidence of any obvious exposure-related effects on male rat brain weights or neuropathology. The most consistent exposure-related effect in the male pups was on the thickness of the corpus callosum, with both the right- and left-sided measures of the thickness of this white matter tract being significantly greater for the male pups in the 0.1 and 1.0 mg/kg-day exposure groups. The behavioral testing suggests prenatal exposure to ammonium perchlorate does not affect the development of gross motor movements in the pups.

scholarly journals The effects of isolates and immune function on hematologic parameters of Blastocystis infection rats

2021 ◽  
Vol 5 (2.1) ◽  
pp. 1
Author(s):  
Ting Deng ◽  
Juan Li ◽  
Xiaohua Li ◽  
Xiaobo Li ◽  
Yiming Yan
Keyword(s):  
Immune Function ◽  
Asymptomatic Carrier ◽  
Symptomatic Patient ◽  
Sprague Dawley ◽  
Blastocystis Hominis ◽  
Infection Models ◽  
The Status ◽  
Blastocystis Sp ◽  
Fully Automatic ◽  
Set Up

Objective: To define a complex of changes in hematologic parameters associated with subtypes (ST) of Blastocystis sp. infections and the status of immune function in Sprague Dawley (SD) rats, and lay the foundation for Blastocystis hominis pathogenesis research. Methods: 5 isolates of ST1, ST3 and ST7 were used, including 1 isolate of ST1 from symptomatic patient, 2 isolates of ST3 and ST7 from symptomatic patients and asymptomatic carrier separately. Immune compromise model was set up using dexamethasone (DEX) and infection models with 5 isolates of ST1, ST3 and ST7, and then examined the hematologic changes post infection 15 days using fully automatic hematology analyzer sysmex xe-2100. Results: The results showed that infections of Blastocystis STs leaded to the increase of platelet indexes including MPV and PDW except ST3 isolated from asymptomatic carrier only with PDW increase and the higher values of PLT in ST7 isolated from asymptomatic carrier compared with the controls in the immune competence status (P < 0.05). However, the infections of Blastocystis ST7 isolated from symptomatic patient gave rise to higher values of WBC, LYMP, EO, MCV and RDW-SD while lower values of NEU% compared with the controls in immune compromise status (P < 0.05). Meanwhile, higher values of WBC and LYMP and lower NEUT% values were observed in ST1 infections compared with the controls (P < 0.05); lower NEUT values in ST1 infections and controls compared with ST3 and ST7 respectively were observed (P < 0.05); the infection of ST3 isolated from symptomatic patient resulted in higher values of MCV and RDW-SD while the asymptomatic isolate of ST3 only had higher RDW-SD (P < 0.05). Conclusion: The virulence of Blastocystis sp. isolated from symptomatic patient is higher than that of the identical subtype one isolated from asymptomatic carrier. The infection of ST7 isolated from symptomatic patients may result in the most distinct hematologic changes among STs, and then followed by ST1 symptomatic isolate. And the severity of Blastocystis sp. infection may be mediated by the immune status of host.

scholarly journals Variable Response of Norepinephrine Transporter to Traumatic Stress and Relationship to Hyperarousal

2021 ◽  
Vol 15 ◽  
Author(s):  
Chiso Nwokafor ◽  
Lidia I. Serova ◽  
Arax Tanelian ◽  
Roxanna J. Nahvi ◽  
Esther L. Sabban
Keyword(s):  
Traumatic Stress ◽  
Neuropsychiatric Symptoms ◽  
Acoustic Startle ◽  
Norepinephrine Transporter ◽  
Brain Regions ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Post Traumatic Stress ◽  
Variable Response ◽  
Western Blots

The noradrenergic systems play a key role in stress triggered disorders such as post-traumatic stress disorder (PTSD). We hypothesized that traumatic stress will alter expression of norepinephrine transporter (NET) in locus coeruleus (LC) and its target brain regions which could be related to hyperarousal. Male Sprague-Dawley rats were subjected to single prolonged stress (SPS) and several weeks later the LC was isolated. NET mRNA levels in LC, determined by RT-PCR, displayed variable response with high and low responsive subgroups. In different cohort, acoustic startle response (ASR) was measured 2 weeks after SPS and levels of NET mRNA and protein in LC determined. The high NET responsive subgroup had greater hyperarousal. Nevertheless, NET protein levels, as determined by western blots, were lower than unstressed controls in LC, ventral hippocampus and medial prefrontal cortex and displayed considerable variability. Hypermethylation of specific CpG region in promoter of SLC6A2 gene, encoding NET, was present in the low, but not high, NET mRNA responsive subgroup. Taken together, the results demonstrate variability in stress elicited changes in NET gene expression and involvement of epigenetic changes. This may underlie mechanisms of susceptibility and resilience to traumatic stress triggered neuropsychiatric symptoms, especially hyperarousal.

scholarly journals Local Anesthesia at ST36 to Reveal Responding Brain Areas todeqi

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Ling-min Jin ◽  
Cai-juan Qin ◽  
Lei Lan ◽  
Jin-bo Sun ◽  
Fang Zeng ◽  
...  
Keyword(s):  
Local Anesthesia ◽  
Primary Motor Cortex ◽  
Superior Temporal Gyrus ◽  
Brain Regions ◽  
Manual Acupuncture ◽  
Brain Areas ◽  
Potential Approach ◽  
Brain Responses ◽  
Set Up ◽  
Significant Activation

Background.Development of non-deqicontrol is still a challenge. This study aims to set up a potential approach to non-deqicontrol by using lidocaine anesthesia at ST36.Methods.Forty healthy volunteers were recruited and they received two fMRI scans. One was accompanied with manual acupuncture at ST36 (DQ group), and another was associated with both local anesthesia and manual acupuncture at the same acupoint (LA group).Results.Comparing to DQ group, more than 90 percentdeqisensations were reduced by local anesthesia in LA group. The mainly activated regions in DQ group were bilateral IFG, S1, primary motor cortex, IPL, thalamus, insula, claustrum, cingulate gyrus, putamen, superior temporal gyrus, and cerebellum. Surprisingly only cerebellum showed significant activation in LA group. Compared to the two groups, bilateral S1, insula, ipsilateral IFG, IPL, claustrum, and contralateral ACC were remarkably activated.Conclusions.Local anesthesia at ST36 is able to block most of thedeqifeelings and inhibit brain responses todeqi, which would be developed into a potential approach for non-deqicontrol. Bilateral S1, insula, ipsilateral IFG, IPL, claustrum, and contralateral ACC might be the key brain regions responding todeqi.

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