Electroencephalographic and histological characteristics of a model of limbic status epilepticus permitting direct control over seizure duration
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Ojbective To study the difference of Aβ 25-35 on neurons between hippocampus and septum. Mdthods employing the method of primary cell culture, neurons survival and SOD were examined ,and amalysed the expression of apoptosis-related gene bcl-xl by Western blot. Result Aβ 25-35 might reduce the survival of hippocampal and septal neurons, increased both activity of CuZn-SOD and expression of Bcl-xl, but decreased the activity of Mn-SOD of hippocampal neurons, and had on obvious effect on septal neurons. Conclusion Aβ 25-35 had the same effect on survival and CuZn-SOD but Mn-SOD between the hippocampus and septum. The cytoxic mechanisms of Aβ 25-35 on hippocampus and septus might be different.
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Neocortex
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The mammalian hippocampal formation (HF) is organized into domains associated with different functions. These differences are driven in part by the pattern of input along the hippocampal long axis, such as visual input to the septal hippocampus and amygdalar input to the temporal hippocampus. HF is also organized along the transverse axis, with different patterns of neural activity in the hippocampus and the entorhinal cortex. In some birds, a similar organization has been observed along both of these axes. However, it is not known what role inputs play in this organization. We used retrograde tracing to map inputs into HF of a food-caching bird, the black-capped chickadee. We first compared two locations along the transverse axis: the hippocampus and the dorsolateral hippocampal area (DL), which is analogous to the entorhinal cortex. We found that pallial regions predominantly targeted DL, while some subcortical regions like the lateral hypothalamus (LHy) preferentially targeted the hippocampus. We then examined the hippocampal long axis and found that almost all inputs were topographic along this direction. For example, the anterior hippocampus was preferentially innervated by thalamic regions, while the posterior hippocampus received more amygdalar input. Some of the topographies we found bear a resemblance to those described in the mammalian brain, revealing a remarkable anatomical similarity of phylogenetically distant animals. More generally, our work establishes the pattern of inputs to HF in chickadees. Some of these patterns may be unique to chickadees, laying the groundwork for studying the anatomical basis of these birds' exceptional hippocampal memory.
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A patient in status epilepticus has continuous or rapidly repeating seizures. Although the danger of this pattern of seizure activity has been recognized since antiquity, our understanding of the pathophysiology of status epilepticus is incomplete. The frequency of cases in the United States is approximately 102,000 to 152,000 per year, and roughly 55,000 deaths are associated with status epilepticus annually.1 Twelve to 30 percent of adult patients with a new diagnosis of epilepsy first present in status epilepticus.2,3 This review focuses on generalized status epilepticus, which is the most common form of the disorder.1,4 This is a life-threatening . . .
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Using quantitative receptor autoradiography, spirodecanone binding was evaluated in the gerbil hippocampus 1 h-1 month after cerebral ischaemia of 10 min. The spirodecanone binding was unaffected in the hippocampus up to 48 h after ischaemia. Thereafter, increased binding was found in the stratum radiatum of hippocampal CA1 sector 7 days and 1 month after ischaemia. Other hippocampal regions showed no significant alterations in the spirodecanone binding. A histological study revealed that the hippocampal CA1 sector was severely damaged 7 days and 1 months after ischaemia. These results demonstrate that spirodecanone binding sites are located on interneurones or glial cells in the hippocampal CA1 sector.
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Objective To study the effects on hippocampal neurons of epilepsy-induced rats with persistent(various) time courses of seizure.Methods 24 SD rats were divided randomly into 4 groups.Three groups of rats were status epilepticus(SE)-induced and differed in seizure-lasting time as follow respectively SE10 min,SE 10-30 min and SE30 min.The fourth was a control group.The ultrastructural morphological changes of hippocampal neuronal cell were observed by electron microscopy;The apoptosis related gene Bcl-2 and Bax proteins in hippocampous were investigated by using immunochemical method and the apoptotic neurons were detected by flow cytometry.Results Little change was seen in the first group,but the hippocampal neurons of the second group had significant apoptotic characters and the neurons showed necrotic features in the third.Conclusions SE triggers hippocampal neuronal degeneration comprised of both types necrosis and apoptosis,but which type is dominant depends on the duration of seizure activity.
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Nonconvulsive status epilepticus includes three clinical situations: complex partial status epilepticus; absence status epilepticus; and obtundation in the presence of electrographic status epilepticus. Animal models that provide information helpful to clinical management exist for both complex partial and absence status epilepticus. In models of complex partial status epilepticus (pilocarpine, kainic acid, and various protocols using electrical stimulation), neuronal damage in discrete neuronal populations follows an episode of status epilepticus. Hippocampal populations are particularly susceptible to neuropathologic sequelae. Although it is difficult in some cases to distinguish whether the inducing agent or the status epilepticus causes neuropathology, the similar patterns of damage caused by different inducing stimuli provide converging lines of evidence suggesting that the neuropathologic consequences stem at least in part from status epilepticus. In models of absence status epilepticus (genetic mutants, pentylenetetrazole), there is relatively scarce neuropathology that can be attributed directly to status epilepticus. Together these data from animal models suggest that neuropathologic consequences from complex partial status epilepticus may be more severe than those from absence status epilepticus. If these findings translate to patients, then nonconvulsive status epilepticus of the complex partial type should be managed more aggressively than nonconvulsive status epilepticus of the absence type.
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In this study, I investigate the role that hippocampal inhibitory cells (intemeurons) have on the synchronization of oscillations between the two hemispheres of the hippocampus. My study focuses in particular on the ripple oscillations, because this network activity is highly synchronous between left and right hippocampus. My hypothesis is that a subset of hippocampal intemeurons might establish axonal connections from the hippocampal area in which the somata reside towards the contralateral side, hence regulating inter-hippocampal ripple discharges. I address this hypothesis injecting in one side of the hippocampus substance P fragment, a peptide that increases the activity of subsets of inhibitory neurons in rat hippocampus, and the antimalarial Quinine whose roles as gap-junction blocker has been well established by numerous publications. Simultaneous recording from both hippocampi are thus compared to investigate whether ipsilateral injected drugs affect hippocampal ripple activity recorded contralaterally. I found that ripple oscillations are indeed affected by injection of the abovementioned drugs: Quinine increases length and decreases Inter Ripple Interval (I.R.I.) in both injected and contralateral hippocampus; on the other hand, SP decreases the average amplitude of the ripple episode, but increases the duration of the ripple event. Most importantly, many of the perturbations observed were preserved between injected and contralateral hippocampus. Since the drugs I employed affect mainly inhibitory neurons, I propose that long-range projecting inhibitory neurons located in the injected hippocampus are responsible for carrying the drugs' effects to the contralateral hippocampus. In conclusion, my results seem to indicate that long-range projecting intemeurons are involved in transmitting ripple synchronization information across the two hippocampi.
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