GABAergic neurons are spared after intrahippocampal kainate in the rat

Davenport, Cynthia J.; Brown, W. J.; Babb, Thomas L.

doi:10.1016/0920-1211(90)90063-2

Cited by 62 publications

(32 citation statements)

References 40 publications

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“…Postmortem studies have suggested that GABA cells in the ACCx of bipolar subjects may fall victim to oxidative stress (Benes et al, 1992;Benes et al, 2000) that occurs in response to excessive amygdalar stimulation (Benes and Beretta, 2001). On the other hand, some studies have paradoxically suggested that GABAergic cells in hippocampus may be resistant to kainic acid -induced excitotoxicity (Davenport et al, 1990), although conflicting results have been reported with less localized applications of kainic acid (Morin et al, 1998). Excessive excitatory activity in nonGABAergic cells could result in consequent changes in oxidative enzymes associated with mitochondria (Benes, 2000;Coyle and Puttfarcken, 1993).…”

Section: Discussionmentioning

confidence: 99%

DNA fragmentation is increased in non-GABAergic neurons in bipolar disorder but not in schizophrenia

Buttner

Bhattacharyya

Walsh

et al. 2007

Schizophrenia Research

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Apoptosis is thought to contribute to neuronal loss in bipolar disorder and schizophrenia, although empiric evidence in support of this idea has been lacking. In this study, we investigated whether or not apoptosis is associated with GABAergic interneurons in the anterior cingulate cortex in schizophrenia (n = 14) and bipolar disorder (n = 14) when compared to normal controls (n = 14). A double-labeling technique using the Klenow method of in situ end-labeling (ISEL) of single-stranded DNA breaks was combined with an in situ hybridization localization of mRNA for the 67 kiloDalton (kDa) isoform of glutamate decarboxylase (GAD67) and applied to the anterior cingulate cortex of 14 normal controls, 14 schizophrenics, and 14 patients with bipolar disorder matched for age and postmortem interval. An increase in Klenow-positive, GAD67-negative nuclei was observed in layer V/VI of patients with bipolar disorder, but not schizophrenics. Klenow-positive cells that were also positive for GAD67 mRNA did not show differences in either patient group. Conclusions: This is the first demonstration that there is more DNA fragmentation in cells showing no detectable GAD67 mRNA in patients with bipolar disorder than in schizophrenics or controls. These findings suggest that non-GABAergic cells may be selectively vulnerable to oxidative stress in patients with bipolar disorder.

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Section: Discussionmentioning

confidence: 99%

DNA fragmentation is increased in non-GABAergic neurons in bipolar disorder but not in schizophrenia

Buttner

Bhattacharyya

Walsh

et al. 2007

Schizophrenia Research

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“…Thus, our finding that prenatal choline supplementation prevented the loss of hippocampal GAD65 protein and mRNA (though not GAD67 response to SE) is particularly interesting. Our findings may represent a protection of GABAergic neurons following SE, although loss of functional inhibition may not be due to a loss of inhibitory neurons per se (Sloviter, 1987;Davenport et al, 1990;Esclapez & Houser, 1999). Rather, a loss in GAD65 expression may contribute to a disruption in GABAergic function, as mice deficient in GAD65 are susceptible to epileptic seizures (Kash et al, 1997).…”

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confidence: 95%

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Wong-Goodrich¹,

Mellott²,

Glenn³

et al. 2008

Neurobiology of Disease

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Prenatal choline supplementation (SUP) protects adult rats against spatial memory deficits observed after excitotoxin-induced status epilepticus (SE). To examine the mechanism underlying this neuroprotection, we determined the effects of SUP on a variety of hippocampal markers known to change in response to SE and thought to underlie ensuing cognitive deficits. Adult offspring from rat dams that received either a Control or SUP diet on embryonic days 12-17 were administered saline or kainic acid (i.p.) to induce SE and were euthanized 16 days later. SUP markedly attenuated seizure-induced hippocampal neurodegeneration, dentate cell proliferation, hippocampal GFAP mRNA expression levels, prevented the loss of hippocampal GAD65 protein and mRNA expression, and altered growth factor expression patterns. SUP also enhanced pre-seizure hippocampal levels of BDNF, NGF, and IGF-1, which may confer a neuroprotective hippocampal microenvironment that dampens the neuropathological response to and/or helps facilitate recovery from SE to protect cognitive function. Keywords choline; kainic acid; hippocampus; seizures; bromodeoxyuridine; growth factor; glutamic acid decarboxylase; glial fibrillary acidic protein; neuroprotection Status epilepticus (SE), a period of prolonged seizures, produces a host of plastic changes in the hippocampus that are thought to contribute to the development of temporal lobe epilepsy. SE results in substantial neuronal loss (Cavazos et al., 1994;Haas et al., 2001;Gorter et al., 2003), γ-aminobutyric acid (GABA) system alterations (e.g., Houser & Esclapez, 1996), reactive gliosis (Jorgensen et al. 1993; Niquet et al., 1994a;Kang et al., 2006), mossy fiber innervation of the dentate gyrus (Sutula et al., 1988;Ben-Ari & Represa, 1990), changes in levels of growth factors (Khrestchatisky et al., 1995;Mudo et al., 1996;Schmidt-Kastner et al., 1996;Shetty et al., 2004), and a transient increase in cell proliferation and neurogenesis (Bengzon et al., 1997;Parent et al., 1997;Scharfman et al., 2000;Hattiangady et al., 2004). These SE-induced degenerative and regenerative changes in the hippocampus are also Corresponding author: Dr. Christina L. Williams, Department of Psychology and Neuroscience, 572 Research Drive, Box 91050, GSRB-II, Room 3022, Duke University, Durham, NC 27708, USA, Phone: 919-660-5638, Fax: 919-660-5798, Email: williams@psych.duke.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. accompanied by deficits in hippocampal-dependent learning and memory (Stafstrom et al., 1993;Liu et al., 1994;Sarkisian et al., 1997;Hort et al., 1999;Mik...

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“…Accordingly, the traditional point of view is that the key intracellular correlate of epileptiform activity, the paroxysmal depolarizing shift (PDS), consists of a giant EPSP (Johnston and Brown 1981) enhanced by activation of voltageregulated intrinsic currents (de Curtis et al 1999;Dichter and Ayala 1987;Prince and Connors 1984;Westbrook and Lothman 1983;Wong and Prince 1978). It was therefore a surprise when more recent evidence showed that synaptic inhibition remains functional in many forms of paroxysmal activities (Cohen et al 2002;Davenport et al 1990;Engel et al 2003;Esclapez et al 1997;Higashima 1988;Prince and Jacobs 1998;Timofeev et al 2002b;Topolnik et al 2003;Traub et al 1996). Also, disruption of inhibitory function does not affect neocortical kindling (Denslow et al 2001), which is associated with an increases in synaptic strength that mediates recruitment of larger cortical areas (Teskey et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Cellular and network mechanisms of electrographic seizures

Bazhenov

Timofeev

Fröhlich

et al. 2008

Drug Discovery Today: Disease Models

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Epileptic seizures constitute a complex multiscale phenomenon that is characterized by synchronized hyperexcitation of neurons in neuronal networks. Recent progress in understanding pathological seizure dynamics provides crucial insights into underlying mechanisms and possible new avenues for the development of novel treatment modalities. Here we review some recent work that combines in vivo experiments and computational modeling to unravel the pathophysiology of seizures of cortical origin. We particularly focus on how activity-dependent changes in extracellular potassium concentration affects the intrinsic dynamics of neurons involved in cortical seizures characterized by spike/wave complexes and fast runs.

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GABAergic neurons are spared after intrahippocampal kainate in the rat

Cited by 62 publications

References 40 publications

DNA fragmentation is increased in non-GABAergic neurons in bipolar disorder but not in schizophrenia

DNA fragmentation is increased in non-GABAergic neurons in bipolar disorder but not in schizophrenia

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Cellular and network mechanisms of electrographic seizures

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