Sub region-specific modulation of synchronous neuronal burst firing after a kainic acid insult in organotypic hippocampal culturesReport as inadecuate




Sub region-specific modulation of synchronous neuronal burst firing after a kainic acid insult in organotypic hippocampal cultures - Download this document for free, or read online. Document in PDF available to download.

BMC Neuroscience

, 9:59

First Online: 02 July 2008Received: 01 November 2007Accepted: 02 July 2008

Abstract

BackgroundExcitotoxicity occurs in a number of pathogenic states including stroke and epilepsy. The adaptations of neuronal circuits in response to such insults may be expected to play an underlying role in pathogenesis. Synchronous neuronal firing can be induced in isolated hippocampal slices and involves all regions of this structure, thereby providing a measure of circuit activity. The effect of an excitotoxic insult kainic acid, KA on Mg-free-induced synchronized neuronal firing was tested in organotypic hippocampal culture by measuring extracellular field activity in CA1 and CA3.

ResultsWithin 24 hrs of the insult regional specific changes in neuronal firing patterns were evident as: i a dramatic reduction in the ability of CA3 to generate firing; and ii a contrasting increase in the frequency and duration of synchronized neuronal firing events in CA1. Two distinct processes underlie the increased propensity of CA1 to generate synchronized burst firing; a lack of ability of the CA3 region to -pace- CA1 resulting in an increased frequency of synchronized events; and a change in the -intrinsic- properties limited to the CA1 region, which is responsible for increased event duration. Neuronal quantification using NeuN immunoflurescent staining and stereological confocal microscopy revealed no significant cell loss in hippocampal sub regions, suggesting that changes in the properties of neurons within this region were responsible for the KA-mediated excitability changes.

ConclusionThese results provide novel insight into adaptation of hippocampal circuits following excitotoxic injury. KA-mediated disruption of the interplay between CA3 and CA1 clearly increases the propensity to synchronized firing in CA1.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2202-9-59 contains supplementary material, which is available to authorized users.

Christopher A Reid, Brendan EL Adams contributed equally to this work.

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Author: Christopher A Reid - Brendan EL Adams - Damian Myers - Terence J O-Brien - David A Williams

Source: https://link.springer.com/







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