Summary:Purpose: Recently the Ca v 2.3 (E/R-type) voltagegated calcium channel (VGCC) has turned out to be not only a potential target for different antiepileptic drugs (e.g., lamotrigine, topiramate) but also a crucial component in the pathogenesis of absence epilepsy, human juvenile myoclonic epilepsy (JME), and epileptiform activity in CA1 neurons. The aim of our study was to perform an electroencephalographic analysis, seizuresusceptibility testing, and histomorphologic characterization of Ca v 2.3 −/− mice to unravel the functional relevance of Ca v 2.3 in ictogenesis.Methods: Generalized and brain-specific Ca v 2.3 knockout animals were analyzed for spontaneous epileptiform discharges by using both electrocorticographic and deep intracerebral recordings. In addition, convulsive seizure activity was induced by systemic administration of either 4-aminopyridine (4-AP; 10 mg/kg, i.p.) or pentylenetetrazol (PTZ; 80 mg/kg, s.c.) to reveal possible alterations in seizure susceptibility. Besides histomorphologic analysis, expression studies of other voltage-gated Ca 2+ channels in Ca v 2.3 −/− brains were carried out by using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR).Results: Both electrocorticographic and deep intrahippocampal recordings exhibited no spontaneous epileptiform discharges indicative of convulsive or nonconvulsive seizure activity during long-term observation. Gross histology and expression levels of other voltage-gated Ca 2+ channels remained unchanged in various brain regions. Surprisingly, PTZ-induced seizure susceptibility was dramatically reduced in Ca v 2.3-deficient mice, whereas 4-AP sensitivity remained unchanged.Conclusions: Ca v 2.3 ablation results in seizure resistance, strongly supporting recent findings in CA1 neurons that Ca v 2.3 triggers epileptiform activity in specialized neurons via plateau potentials and afterdepolarizations. We provide novel insight into the functional involvement of Ca v 2.3 in ictogenesis and seizure susceptibility on the whole-animal level.

Voltage-gated calcium channels are key components in the etiology and pathogenesis of epilepsies. Former studies mainly focused on P/Q-type Ca(v)2.1 and T-type Ca(v)3.2 Ca(2+) channels involved in absence epileptogenesis, but recent findings also point to an intriguing role of the Ca(v)2.3 E/R-type Ca(2+) channel in ictogenesis and seizure propagation. Based on the observation that Ca(v)2.3 is thought to induce plateau potentials in CA1 pyramidal cells, which can trigger epileptiform activity, our recent investigation revealed reduced PTZ-seizure susceptibility and altered seizure architecture in Ca(v)2.3(-/-) mice compared with controls. In the present study we tested hippocampal seizure susceptibility in Ca(v)2.3-deficient mice using surface and deep intrahippocampal telemetric EEG recordings as well as phenotypic seizure video analysis. Administration of kainic acid (30 mg/kg ip) revealed clear alteration in behavioral seizure architecture and dramatic resistance to limbic seizures in Ca(v)2.3(-/-) mice compared with controls, whereas no difference in hippocampal EEG seizure activity between both genotypes could be detected at this suprathreshold dosage. The same tendency was observed for NMDA seizure susceptibility (150 mg/kg ip) approaching the level of significance. In addition, histochemical analysis within the hippocampus revealed that excitotoxic effects after kainic acid administration are absent in Ca(v)2.3(-/-) mice, whereas Ca(v)2.3(+/+) animals exhibited clear and typical signs of excitotoxic cell death. These findings clearly indicate that the Ca(v)2.3 voltage-gated calcium channel plays a crucial role in both hippocampal ictogenesis and seizure generalization and is of central importance in neuronal degeneration after excitotoxic events.

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Multiple types of voltage-activated Ca2+ channels (T, L, N, P, Q, R type) coexist in excitable cells and participate in synaptic differentiation, secretion, transmitter release, and neuronal plasticity. Ca2+ ions entering cells trigger these events through their interaction with the ion channel itself or through Ca2+ binding to target proteins initiating signalling cascades at cytosolic loops of the ion conducting subunit (Cava1). These loops interact with target proteins in a Ca2+-dependent or independent manner. In Cav2.3-containing channels the cytosolic linker between domains II and III confers a novel Ca2+ sensitivity to E-type Ca2+ channels including phorbol ester sensitive signalling via protein kinase C (PKC) in Cav2.3 transfected HEK-293 cells. To understand Ca2+ and phorbol ester mediated activation of Cav2.3 Ca2+ channels, protein interaction partners of the II-III loop were identified. FLAG-tagged II-III - loop of human Cav2.3 was over-expressed in HEK 293 cells, and the molecular chaperone hsp70, which is known to interact with PKC, was identified as a novel functional interaction partner. Immunopurified II-III loop-protein of neuronal and endocrine Cav2.3 splice variants stimulate autophosphorylation of PKCa, leading to the suggestion that hsp70 - binding to the II-III loop - may act as an adaptor for Ca2+ dependent targeting of PKC to E-type Ca2+ channels.

Smart agriculture has been a promising model with the intention of supervising farms by means of contemporary wireless technologies to enhance the quantity and quality of yield at the same time as minimizing the individual labor requirement. In addition the effective utilization of the Sensors as communication components that is the key one to monitor and manage soil, water, light, humidity, temperature. A Mobile Ad-hoc sensor node comprises sensors to gather real time environment from the agricultural land with the wireless communication technology and process the data before sharing information with other nodes in the network. On the other hand, the challenges have been enormously high path loss and lack of communication range under the environment when passing through soil, sand, water and other climatic conditions. As Wireless Sensor Networks (WSNs) has self-organized and adhoc wireless capability to monitor physical or environmental conditions, it can be used effectively in smart agriculture. As sensor nodes have been limited itself by means of power to be in active mode always, the design of such energy e cient Agriculture WSN is a paramount issue. Hence it has been planned to utilize the WSN as well as Ubiquitous technology for the smart agriculture with energy e ciency. With the purpose of build up a model, a Ubiquitous agriculture Mobile Sensor Network based Threshold built-in MAC Routing protocol (TBMP) has been proposed to make it t for minimal resource utilization by comparing with the existing protocols IMR and PTSR. In addition, the testing will be done to monitor changes in environmental surroundings in the agricultural land smartly in order to obtain maximum usage of Ubiquitous concept by applying existing and proposed protocols.

Background: Earlier, we showed that nicotinamide (NAM) treatment impairs spatial memory through the downregulation of CREB-Sirt 1-brain-derived neurotrophic factor (Bdnf) signaling cascade. Purpose: In this study, we examine whether NAM treatment alters CREB-regulated genes through ­microRNAs. Method: To test this hypothesis, goldfish (Carassius auratus) were divided into 2 groups: (i) vehicle group (VEH; double distilled water intra-peritoneally [i.p.]) (ii) nicotinamide group (NAM, 1,000 mg/kg, i.p.) and again divided into VEH untrained/trained, NAM untrained/trained. One hour after receiving VEH or NAM, individuals were subject to contextual fear conditioning (CFC) training. After 24 h, both the groups were tested for contextual fear memory. Subsequently, miR-132/212 levels, regulated immediate-early genes (IEGs: C-fos and EGR-1) and Bdnf but not its receptor. ­TrkB1were examined following 0’ and 60’ min after training, and compared with the untrained group. Results: We observed that NAM treatment significantly impaired fear memory. Further, the analysis showed that miR-132 level was not altered, but miR-212 level was significantly upregulated after CFC training only in NAM-treated fish. We also found that NAM treatment downregulated IEGs and Bdnf but not its receptor TrkB1. Conclusions: Present study suggests that NAM-treatment impaired fear memory and control IEGs, Bdnf and TrkB1 expression by differentially regulating miR-132 and 212.

The high prevalence of urban flooding in the world is increasing rapidly with the rise in extreme weather events. Consequently, this research uses an Automatic Flood Monitoring System (ARMS) through a video surveillance camera. Initially, videos are collected from a surveillance camera and converted into video frames. After converting the video frames, the water level can be identified by using a Histogram of oriented Gradient (HoG), which is used to remove the functionality. Completing the extracted features, the frames are enhanced by using a median filter to remove the unwanted noise from the image. The next step is water level classifiers using a Convolutional Neural Network (CNN), which is utilized to classify the water level in the images. The performance analysis of the method is analyzed by various parameters. The accuracy of the proposed method is 11% higher than that of the k-Nearest Neighbors (KNN) classifiers and 5% higher than that of the ANN classifiers, and the processing time is 7% less than that of the KNN classifiers and 4% less than that of the Artificial Neural Network (ANN) classifiers.

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