Mohammed Mostafizur Rahman

Neighborhood matters: divergent patterns of stress-induced plasticity across the brain

The fact that exposure to severe stress leads to the development of psychiatric disorders serves as the basic rationale for animal models of stress disorders. Clinical and neuroimaging studies have shown that three brain areas involved in learning and memory—the hippocampus, amygdala and prefrontal cortex—undergo distinct structural and functional changes in individuals with stress disorders. These findings from patient studies pose several challenges for animal models of stress disorders. For instance, why does stress impair cognitive function, yet enhance fear and anxiety? Can the same stressful experience elicit contrasting patterns of plasticity in the hippocampus, amygdala and prefrontal cortex? How does even a brief exposure to traumatic stress lead to long-lasting behavioral abnormalities? Thus, animal models of stress disorders must not only capture the unique spatio-temporal features of structural and functional alterations in these brain areas, but must also provide insights into the underlying neuronal plasticity mechanisms. This Review will address some of these key questions by describing findings from animal models on how stress-induced plasticity varies across different brain regions and thereby gives rise to the debilitating emotional and cognitive symptoms of stress-related psychiatric disorders.

Trivalent Y3+ ionic sensor development based on (E)-Methyl-N′-nitrobenzylidene-benzenesulfonohydrazide (MNBBSH) derivatives modified with nafion matrix

Abstract(E)-Methyl-N′-nitrobenzylidene-benzenesulfonohydrazide (MNBBSH) compounds were synthesized using a condensation procedure from the derivatives of nitrobenzaldehyde and 4-Methyl-benzenesulfonylhydrazine, which crystallized in ethanol and methanol as well as characterized by FTIR, UV-Vis, 1H-NMR, and 13C-NMR. MNBBSH structure was confirmed using a single crystal X-ray diffraction technique and used for the detection of selective yttrium ion (Y3+) by I-V system. A thin layer of MNBBSH was deposited onto a glassy carbon electrode (GCE) with 5% nafion for the sensitive and selective Y3+ sensor. The modified MNBBSH/GCE sensor is exhibited the better electrochemical performances such as sensitivity, limit of detection (LOD), linear dynamic range (LDR), limit of quantification (LOQ), short response time, and long term storage ability towards the selective metal ion (Y3+). The calibration curve of 2-MNBBSH/GCE sensor was plotted at +1.1 V over a broad range of Y3+ concentration. Sensitivity, LOD, LDR and LOQ of the fabricated sensor towards Y3+ were calculated from the calibration curve and found as 1.90 pAμM−1 cm−2, 10.0 pM, 1.0 nM~1.0 mM and 338.33 mM respectively. The 2-MNBBSH/Nafion/GCE sensor was applied to the selective determination of Y3+ in spiked samples such as industrial effluent and real water samples from different sources, and found acceptable and reasonable results.

Chronic immobilization stress occludes in vivo cortical activation in an animal model of panic induced by carbon dioxide inhalation.

Breathing high concentrations of carbon dioxide (CO2) can trigger panic and anxiety in humans. CO2 inhalation has been hypothesized to activate neural systems similar to those underlying fear learning, especially those involving the amygdala. Amygdala activity is also upregulated by stress. Recently, however, a separate pathway has been proposed for interoceptive panic and anxiety signals, as patients exhibited CO2-inhalation induced panic responses despite bilateral lesions of the amygdala. This paradoxical observation has raised the possibility that cortical circuits may underlie these responses. We sought to examine these divergent models by comparing in vivo brain activation in unstressed and chronically-stressed rats breathing CO2. Regional cerebral blood flow measurements using functional Magnetic Resonance Imaging (fMRI) in lightly-anaesthetized rats showed especially strong activation of the somatosensory cortex by CO2 inhalation in the unstressed group. Strikingly, prior exposure to chronic stress occluded this effect on cortical activity. This lends support to recent clinical observations and highlights the importance of looking beyond the traditional focus on limbic structures, such as the hippocampus and amygdala, to investigate a role for cortical areas in panic and anxiety in humans.

Fabrication of 1,4-dioxane sensor based on microwave assisted PAni-SiO2 nanocomposites

In this study, conducting polyaniline (PAni) and silicon dioxide (SiO2) nanocomposites (NCs) were synthesized for chemical sensing applications by microwave assisted reaction technique. Facile synthesis and characterization of the PAni-SiO2 nanocomposites were investigated in details and discussed in this report. For the potential application, 1,4-dioxane chemical sensor was fabricated with the PAni-SiO2 nanocomposites deposited onto glassy carbon electrode (GCE). A very thin uniform film was deposited onto GCE with nanocomposite by using conducting 5% nafion binder at room conditions. To evaluate the sensor analytical performances, a calibration plot such as current versus concentration of 1,4-dioxane was drawn and calculated the analytical parameters from the slope of calibration curve. Results are found as sensitivity (0.5934 µAµmol-1 L-2 cm-2), detection limit (16.0 ± 0.8 pmol L-1), and quantification limit (LOQ; 53.3 ± 1.5 pmol L-1) in this observation. Considering the linear region in calibration plot, the linear dynamic range of 1,4-dioxane chemical sensor was found (0.12 nmol L-1 ∼ 1.2 mmol L-1). Besides this, the proposed 1,4-dioxane chemical sensor was exhibited good reproducibility, long-term stability, high accuracy in detecting of 1,4-dioxane in real environmental samples. This research is to develop of a selective and an efficient electrochemical sensor. It might be a simple and easy way by applying electrochemical method to ensure the safe and sustainable green environment.

Extinction recall of fear memories formed before stress is not affected despite higher theta activity in the amygdala

Stress is known to exert its detrimental effects not only by enhancing fear, but also by impairing its extinction. However, in earlier studies stress exposure preceded both processes. Thus, compared to unstressed animals, stressed animals had to extinguish fear memories that were strengthened by prior exposure to stress. Here, we dissociate the two processes to examine if stress specifically impairs the acquisition and recall of fear extinction. Strikingly, when fear memories were formed before stress exposure, thereby allowing animals to initiate extinction from comparable levels of fear, recall of fear extinction was unaffected. Despite this, we observed a persistent increase in theta activity in the BLA. Theta activity in the mPFC, by contrast, was normal. Stress also disrupted mPFC-BLA theta-frequency synchrony and directional coupling. Thus, in the absence of the fear-enhancing effects of stress, the expression of fear during and after extinction reflects normal regulation of theta activity in the mPFC, not theta hyperactivity in the amygdala.

Extinction recall of fear memories formed before stress is not affected despite amygdalar hyperactivity

Stress is known to exert its detrimental effects not only by enhancing fear, but also by impairing its extinction. However, in earlier studies stress exposure invariably preceded both processes. Thus, compared to unstressed animals, stressed animals had to extinguish fear memories from higher levels of freezing caused by prior exposure to stress. Here we decouple the two processes to examine if stress specifically impairs fear extinction. Strikingly, when fear memories were formed before stress exposure, thereby allowing animals to initiate extinction from comparable levels of fear, recall of fear extinction was unaffected. Despite this we observed a persistent increase in theta activity in the BLA. Theta activity in the mPFC, by contrast, was normal. Stress also disrupted mPFC-BLA theta-frequency synchrony and directional coupling. Thus, in the absence of the fear-enhancing effects of stress, the expression of fear reflects normal regulation of mPFC activity, not stress-induced hyperactivity in the amygdala.

Activation of the same mGluR5 receptors in the amygdala causes divergent effects on specific versus indiscriminate fear

Although mGluR5-antagonists prevent fear and anxiety, little is known about how the same receptor in the amygdala gives rise to both. Combining in vitro and in vivo activation of mGluR5 in rats, we identify specific changes in intrinsic excitability and synaptic plasticity in basolateral amygdala neurons that give rise to temporally distinct and mutually exclusive effects on fear-related behaviors. The immediate impact of mGluR5 activation is to produce anxiety manifested as indiscriminate fear of both tone and context. Surprisingly, this state does not interfere with the proper encoding of tone-shock associations that eventually lead to enhanced cue-specific fear. These results provide a new framework for dissecting the functional impact of amygdalar mGluR-plasticity on fear versus anxiety in health and disease. DOI: http://dx.doi.org/10.7554/eLife.25665.001

Elucidating Variants in Systemic JIA from Analysis of Illumina & Ion Torrent Exome Data

Motivation Children with systemic juvenile idiopathic arthritis (SJIA) are affected by a wide-range of complications. Partially arising from the difficulty of diagnosis due to the idiopathic nature of the indication. There may be a genetic basis for SJIA, which could help in both diagnosis, and treatment. Results Two mutations in the Fc epsilon RI pathway, including PIK3CD, were detected in low-coverage Ion Torrent data. Variants of unknown significance were detected within HLA regions on standard Illumina exomes. CSF2RA, which could account for pulmonary observations, had insignificant coverage on both datasets. Availability ftp.systemicjia.com Contact mo@genedrop.com