Altered NR2A/NR2B ratio in hippocampus of spatial learning-impaired aged rats

The activation of the N-methyl-D-aspartate receptor (NMDAR) is critical for the induction of synaptic plasticity in the hippocampus. Aging can alter glutamatergic synaptic transmission in the hippocampus, and cognitive impairments in aged animals are accompanied by reduced NMDARmediated plasticity at Schaffer collateral—CA1 synapses. However, the specific contribution of NMDAR subunits to NMDAR-mediated synaptic responses in aged tissue has not yet been fully understood. The main purpose of present study was to examine whether there is an impact of aging on NMDAR subunit expression and whether synaptic plasticity may depend on NMDAR subunit composition in the aged hippocampus

Altered NR2A/NR2B ratio in hippocampus of spatial learning-impaired aged rats

The activation of the N-methyl-D-aspartate receptor (NMDAR) is critical for the induction of synaptic plasticity in the hippocampus. Aging can alter glutamatergic synaptic transmission in the hippocampus, and cognitive impairments in aged animals are accompanied by reduced NMDARmediated plasticity at Schaffer collateral—CA1 synapses. However, the specific contribution of NMDAR subunits to NMDAR-mediated synaptic responses in aged tissue has not yet been fully understood. The main purpose of present study was to examine whether there is an impact of aging on NMDAR subunit expression and whether synaptic plasticity may depend on NMDAR subunit composition in the aged hippocampus

PRODUCTION RENDERING ON A LOCAL AREA NETWORK

The production of a computer animation is a computational demanding task, specially when we are rendering complex scenes with features such as anti-aliasing, shadowing, texturing, reflections, and refractions. Depending on the complexity and duration of the animation, the generation of all images with full resolution and high quality can take days, weeks, even months. The use of a distributed renderer running on a network of workstations is a cost-effective solution that not only shortens the processing time, but also to improves the reliability of the system. In this paper, we describe our approach to the problem, stressing in particular the load balancing and error recovery strategies of our solution.16331732

Antiepileptic drugs abolish ictal but not interictal epileptiform discharges in vitro

Purpose: We established the effects of the antiepilepticdrugs (AEDs) carbamazepine (CBZ), topiramate(TPM), and valproic acid (VPA) on theepileptiform activity induced by 4-aminopyridine(4AP) in the rat entorhinal cortex (EC) in anin vitro brain slice preparation.Methods: Brain slices were obtained from Sprague-Dawley rats (200–250 g). Field and intracellularrecordings were made from the EC during bathapplication of 4AP (50 microM). AEDs, and in someexperiments, picrotoxin were bath applied concomitantly.Results: Prolonged (>3 s), ictal-like epileptiformevents were abolished by CBZ (50 microM), TPM(50 microM), and VPA (1 mM), whereas shorter (<3 s)interictal-like discharges continued to occur, evenat concentrations up to 4-fold as high. gamma-Aminobutyricacid (GABA)A–receptor antagonism changedthe 4AP-induced activity into recurrent interictallikeevents that were not affected by CBZ or TPM,even at the highest concentrations. To establishwhether these findings reflected the temporal featuresof the epileptiform discharges, we testedCBZ and TPM on 4AP-induced epileptiform activitydriven by stimuli delivered at 100-, 10-, and 5-sintervals; these AEDs reduced ictal-like responsesto stimuli at 100-s intervals at nearly therapeuticconcentrations, but did not influence shorter interictal-like events elicited by stimuli deliveredevery 10 or 5 s.Conclusions: We conclude that the AED ability tocontrol epileptiform synchronization in vitrodepends mainly on activity-dependent characteristicssuch as discharge duration. Our data are inkeeping with clinical evidence indicating that interictalactivity is unaffected by AED levels that areeffective to stop seizures

Network and pharmacological mechanisms leading to epileptiform synchronization in the limbic system in vitro

Seizures in patients presenting with mesial temporal lobe epilepsy result from the interaction among neuronal networks in limbic structures such as the hippocampus, amygdala and entorhinal cortex. Mesial temporal lobe epilepsy, one of the most common forms of partial epilepsy in adulthood, is generally accompanied by a pattern of brain damage known as mesial temporal sclerosis. Limbic seizures can be mimicked in vitro using preparations of combined hippocampus-entorhinal cortex slices perfused with artificial cerebrospinal fluid containing convulsants or nominally zero Mg2+, in order to produce epileptiform synchronization. Here, we summarize experimental evidence obtained in such slices from rodents. These data indicate that in control animals: (i) prolonged, NMDA receptor-dependent epileptiform discharges, resembling electrographic limbic seizures, originate in the entorhinal cortex from where they propagate to the hippocampus via the perforant path-dentate gyrus route; (ii) the initiation and maintenance of these ictal discharges is paradoxically contributed by GABA (mainly type A) receptor-mediated mechanisms; and (iii) CA3 outputs, which relay a continuous pattern of interictal discharge at approximately 1 Hz, control rather than sustain ictal discharge generation in entorhinal cortex. Recent work indicates that such a control is weakened in the pilocarpine model of epilepsy (presumably as a result of CA3 cell damage). In addition, in these experiments electrographic seizure activity spreads directly to the CA1-subiculum regions through the temporoammonic pathway. Studies reviewed here indicate that these changes in network interactions, along with other mechanisms of synaptic plasticity (e.g. axonal sprouting, decreased activation of interneurons, upregulation of bursting neurons) can confer to the epileptic, damaged limbic system, the ability to produce recurrent limbic seizures as seen in patients with mesial temporal lobe epilepsy. (C) 2002 Elsevier Science Ltd. All rights reserved

Phase-locking characteristics of limbic P3 responses in hippocampal sclerosis.

Contains fulltext : 49135.pdf (Publisher’s version ) (Closed access)Amplitudes of the P3 recorded invasively from the medial temporal lobe (MTL-P3) have been reported to be reduced on the side of a mediotemporal epileptogenic focus. This reduction has been attributed to the massive cell loss within the hippocampus associated with hippocampal sclerosis. It has remained unclear how functional connectivity between the hippocampus and rhinal cortex, as well as within the hippocampus, is altered in hippocampal sclerosis. To investigate this issue, we analyzed to what extent stimulus-related phase-locking and power changes within the low-frequency range (2-30 Hz) and within the gamma band (32-48 Hz), as well as rhinal-hippocampal phase synchronization contribute to the averaged MTL-P3 potentials. Event-related responses were recorded via bilateral depth electrodes in epilepsy patients with unilateral hippocampal sclerosis, who performed a visual oddball experiment. On the contralateral (nonsclerotic) side, successful target detection was associated with an increase of power and phase locking of hippocampal activity in both the low-frequency range and in the gamma range. Besides, there were rhinal-hippocampal synchronization enhancements in the theta and gamma range. On the ipsilateral (sclerotic) side, the event-related power increase in the low-frequency range had almost disappeared, a finding likely to be explained by the loss of principle neurons. However, low-frequency phase-locking, rhinal-hippocampal synchronization, as well as event-related power changes in the gamma range persisted ipsilaterally, although there were differences in temporal and spectral characteristics. These findings support the hypothesis that functional connectivity between hippocampus and rhinal cortex, as well as intrahippocampal connectivity, are partially preserved in hippocampal sclerosis

Soft tempest: Hidden data transmission using electromagnetic emanations

Abstract. It is well known that eavesdroppers can reconstruct video screen content from radio frequency emanations. We discuss techniques that enable the software on a computer to control the electromagnetic radiation it transmits. This can be used for both attack and defence. To attack a system, malicious code can encode stolen information in the machine’s RF emissions and optimise them for some combination of reception range, receiver cost and covertness. To defend a system, a trusted screen driver can display sensitive information using fonts which minimise the energy of these emissions. There is also an interesting potential application to software copyright protection.