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Byline: George K. Kostopoulos This paper presents a review of e-government initiatives in the Arabian Gulf, where extensive efforts are being made to capitalise on the cyber technologies in order to enhance the government to citizen service. The described cases are from Kuwait, Bahrain, Saudi Arabia, Qatar, the United Arab Emirates and Oman. The collective message delivered by the examined cases is that e-government is becoming an integral part of the respective countries' life, with a by-product being an increase in the society's cyber-literacy. The dual mission of the Dubai e-government is: 'To ease the lives of people and business interacting with government, and to contribute in establishing Dubai as a leading economic hub.' oSheikh Mohammed Bin Rashid Al Maktoum.

Byline: George Kostopoulos In this paper, socio-techno-educational trends and the resulting issues are discussed. The need for curricula management is pointed out and specific areas are identified. The paper's thesis is that, at the undergraduate degree level, four courses need be included on the utilisation of cyberpower, while at the individual course level, the syllabi must contain deliverables that are web-researched and web-presentable. In addition, the student-faculty response time needs to be minimised to maintain an efficient and effective teaching-learning environment.

Mounting evidence for the role of sleep spindles in neuroplasticity has led to an increased interest in these non-rapid eye movement (NREM) sleep oscillations. It has been hypothesized that fast and slow spindles might play a different role in memory processing. Here, we present a new sleep spindle detection algorithm utilizing a continuous wavelet transform (CWT) and individual adjustment of slow and fast spindle frequency ranges. Eighteen nap recordings of ten subjects were used for algorithm validation. Our method was compared with both a human scorer and a commercially available SIESTA spindle detector. For the validation set, mean agreement between our detector and human scorer measured during sleep stage 2 using kappa coefficient was 0.45, whereas mean agreement between our detector and SIESTA algorithm was 0.62. Our algorithm was also applied to sleep-related memory consolidation data previously analyzed with a SIESTA detector and confirmed previous findings of significant correlation between spindle density and declarative memory consolidation. We then applied our method to a study in monozygotic (MZ) and dizygotic (DZ) twins, examining the genetic component of slow and fast sleep spindle parameters. Our analysis revealed strong genetic influence on variance of all slow spindle parameters, weaker genetic effect on fast spindles, and no effects on fast spindle density and number during stage 2 sleep. [ABSTRACT FROM AUTHOR]

Summary: Although adenosine is widely assumed to be an endogenous anticonvulsant its role in epileptogenesis is still contradictory. Using slices from the dorsal (DH) and the vental (VH) rat hippocampus and extracellular recordings from the CA3 field we aimed to determine the effects of endogenous adenosine on the expression and long-term maintenance of epileptiform activity induced by blockade of adenosine receptors types A1 (A1R) and A2 (A2R) under conditions of low magnesium. We found that the A1Rs blockade induced persistent epileptiform discharges (PED) more frequently in VH (by 52%) than in DH (by 31%). The induction of PED upon an additional blockade of A2Rs increased in VH (by 48%) but decreased in DH (by 74%). Remarkably, the increment in VH was prevented by a blockade of NMDARs. A blockade of A2Rs increased the NMDAR-mediated component of evoked synaptic potential in both VH and DH (by ∼100%) but suppressed the non-NMDAR-mediated component in DH but not VH. A blockade of A1Rs induced PED equally in DH (76%) and VH (80%) via a NMDAR-independent mechanism. A blockade of A2Rs under blockade of A1Rs and NMDARs reduced the PED to 17% in DH and to 38% in VH. These findings show that A2Rs play a different role in the long-term maintenance of epileptiform activity between DH and VH and suggest that endogenous activation of A2Rs facilitates NMDAR-independent induction of PED in both hippocampal poles, but suppresses NMDAR-dependent induction of PED in VH. [ABSTRACT FROM AUTHOR]

Hippocampal functions appear to be segregated along the dorso-ventral axis of the structure. Differences at the cellular and local neuronal network level may be involved in this functional segregation. In this study the characteristics of CA1 recurrent inhibition (RI) were measured and compared between dorsal (DH, n = 95) and ventral (VH, n = 60) hippocampal slices, using recordings of suprathreshold field potentials. RI strength was estimated as the percentile decrease of the population spike (PS) amplitude evoked with an orthodromic stimulus (at the Schaffer collaterals) when preceded by an antidromic stimulus (at the alveus). Varying the interpulse interval (IPI) between the two stimuli, we estimated RI duration. Alvear stimulation produced significant PS suppression in both VH and DH at every IPI tested, from 10 to 270 ms. Moreover, gradually more oblique DH (but not VH) slices displayed increasing RI, which at IPIs ≤125 ms was reversibly abolished by the GABAA receptor antagonist picrotoxin (10 μM). The GABAA-mediated RI, measured under the blockade of GABAB receptors, was weaker, decayed faster and lasted less in VH compared to DH slices, regardless of the slice orientation. Specifically, in VH compared to DH, the PS suppression at 20 ms was 34.4 ± 4.5% versus 69.9 ± 6.5% ( P < 0.001), the time constant of RI decay was 29 ± 2.4 versus 87.5 ± 13.6 ms ( P < 0.01) and the duration was 50 versus 125 ms ( P < 0.001). Thus, GABAA-mediated RI may control the CA1 excitatory output less effectively in VH compared to DH. The observed dorso-ventral differences in RI contribute to the longitudinal diversification of the structure and may underlie to some extent the region-specificity of hippocampal functions. [ABSTRACT FROM AUTHOR]

The present study shows that adult rat transverse slices from the ventral hippocampus perfused with standard medium persistently generate spontaneous synchronous field potentials. In CA1 st. pyramidale this regular ventral hippocampus spontaneous synchronous activity (VHSSA) was positive with mean amplitude 0.18±0.02 mV (n=80 slices) and occurred every 0.48±0.02 s. Simultaneous intracellular recordings from CA1 pyramidal neurons demonstrated that concomitant hyperpolarizations invariably occurred in association to this field activity and could thus constitute its electrical generators. These hyperpolarizations, had mean amplitude 2.7±0.6 mV, duration at half amplitude 44.8±6.6 ms, they reversed at −72.6±1.5 mV (n=10 cells), they effectively suspended the depolarization-induced tonic neuronal firing of all ten pyramidal neurons and they were reversibly abolished, together with field potentials, by the GABAA receptor antagonist bicuculline (5 μM, n=4). VHSSA was also dependent on fast glutamatergic transmission, since it was blocked by the antagonist of AMPA/kainate receptors 6-Cyano-7-nitroquinoxaline-2,3-dione disodium (10 μM, n=3). We propose that, under standard in vitro conditions, synchronous GABAA-mediated hyperpolarizing potentials are spontaneously generated in pyramidal neurons presumably resulting from the phasic quasi-rhythmic discharge of a local interneuronal network of ventral hippocampus. [Copyright &y& Elsevier]

This study demonstrates that transverse slices taken from the ventral hippocampus of adult rats perfused with a medium of normal ionic composition sustain spontaneous periodic field potentials due to the synchronous activity of a population of neurons. This ventral hippocampus spontaneous synchronous activity (VHSSA) in CA1 stratum pyramidale consisted of positive potentials (∼0.12 mV, 55 ms) occurring at a frequency of 2.8 ± 0.2 Hz for hours without interruption. VHSSA was most frequently observed in slices taken 1–3 mm from the ventral end of hippocampus, and was absent in slices taken from tissue more than 4.5 mm away from it. Stimulation of Schaffer collaterals primed the appearance of potentials, which were similar to VHSSA and clearly distinguishable from excitatory postsynaptic potentials. In view of the known relative proneness of ventral hippocampus to epilepsy, we perfused ventral slices with high-[K+]o medium (8 mM). Albeit reduced in amplitude, VHSSA persisted during the high-[K+]o induced interictal-like epileptiform activity. We could not document any temporal relationship between the two phenomena. Low concentrations of the antagonist of γ-amino-butyric acid receptors, type A, bicuculline (2–3 μM), which enhanced the high-[K+]o induced epileptiform activity, reversibly blocked the VHSSA. We conclude that under standard in vitro conditions small circuits in the ventral hippocampus are most often and for long periods of time engaged in synchronous quasi-rhythmic low-frequency activity, generated locally by mechanisms substantially differing from those supporting epileptiform discharges. [Copyright &y& Elsevier]