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      Neuropeptide Y affects thalamic reticular nucleus neuronal firing and network synchronization associated with suppression of spike-wave discharges

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          Pathophysiological mechanisms of genetic absence epilepsy in the rat.

          Generalized non-convulsive absence seizures are characterized by the occurrence of synchronous and bilateral spike and wave discharges (SWDs) on the electroencephalogram, that are concomitant with a behavioral arrest. Many similarities between rodent and human absence seizures support the use of genetic rodent models, in which spontaneous SWDs occur. This review summarizes data obtained on the neurophysiological and neurochemical mechanisms of absence seizures with special emphasis on the Genetic Absence Epilepsy Rats from Strasbourg (GAERS). EEG recordings from various brain regions and lesion experiments showed that the cortex, the reticular nucleus and the relay nuclei of the thalamus play a predominant role in the development of SWDs. Neither the cortex, nor the thalamus alone can sustain SWDs, indicating that both structures are intimely involved in the genesis of SWDs. Pharmacological data confirmed that both inhibitory and excitatory neurotransmissions are involved in the genesis and control of absence seizures. Whether the generation of SWDs is the result of an excessive cortical excitability, due to an unbalance between inhibition and excitation, or excessive thalamic oscillations, due to abnormal intrinsic neuronal properties under the control of inhibitory GABAergic mechanisms, remains controversial. The thalamo-cortical activity is regulated by several monoaminergic and cholinergic projections. An alteration of the activity of these different ascending inputs may induce a temporary inadequation of the functional state between the cortex and the thalamus and thus promote SWDs. The experimental data are discussed in view of these possible pathophysiological mechanisms.
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            Ethosuximide, valproic acid, and lamotrigine in childhood absence epilepsy: initial monotherapy outcomes at 12 months.

            Determine the optimal initial monotherapy for children with newly diagnosed childhood absence epilepsy (CAE) based on 12 months of double-blind therapy.
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              Burst and oscillation as disparate neuronal properties.

              We have developed methods to detect and discern burst and oscillatory patterns of neuronal activity. In them, a burst period is defined as an interval in which there are a significantly higher number of spikes as compared to other intervals in the spike train. Oscillation is defined as a spike train in which significant periodicity is detected in its autocorrelogram. The main feature of our burst detection method is that discharge density (i.e., the number of spikes in a short interval) is used instead of the interspike interval. This enables one to assess the likelihood of having burst periods in a spike train. We use the Lomb periodogram to detect periodicity in an autocorrelogram. This method gives one significance of periodicity detected and enables the detection of multiple frequencies in an autocorrelogram. The advantage of these methods is discussed in comparison with the other methods used to detect bursting and oscillatory activity.
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                Author and article information

                Journal
                Epilepsia
                Epilepsia
                Wiley
                00139580
                July 2018
                July 2018
                June 20 2018
                : 59
                : 7
                : 1444-1454
                Affiliations
                [1 ]Department of Medicine; The Royal Melbourne Hospital; University of Melbourne; Parkville Vic. Australia
                [2 ]Departments of Neuroscience and Neurology; Central Clinical School; The Alfred Hospital; Monash University; Melbourne Vic. Australia
                [3 ]Department of Physiology and Pharmacology; The University of New South Wales; Randwick NSW Australia
                Article
                10.1111/epi.14451
                0fcedbf6-7d73-44c3-be16-193f2f81ea27
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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