Resistance of the immature hippocampus to seizure-induced synaptic reorganization

Sperber, Ellen F.; Haas, Kurt; Stanton, Patric K.; Moshé, Solomon L.

doi:10.1016/0165-3806(91)90158-f

Cited by 236 publications

(155 citation statements)

References 43 publications

Supporting

Mentioning

140

Contrasting

Unclassified

Order By: Relevance

“…At P10, status epilepticus induced no cell loss in any region or at any time examined (24 hr and 30 d) after status epilepticus (data not illustrated). These age-related differences in patterns of neurodegeneration observed in status epilepticus rats confirm previous studies of Ben-Ari (1985) and Sperber et al (1991).…”

Section: Status Epilepticus Induces Neurodegeneration In Adult But Nosupporting

confidence: 79%

Status Epilepticus-Induced Alterations in Metabotropic Glutamate Receptor Expression in Young and Adult Rats

et al. 1997

View full text Add to dashboard Cite

In adult rats, kainic acid induces status epilepticus and delayed, selective cell loss of pyramidal neurons in the hippocampal CA3. In pup rats, kainate induces status epilepticus but not the accompanying neuronal cell death. The precise mechanisms underlying this age-dependent vulnerability to seizure-induced cell death are not understood. Metabotropic glutamate receptors (mGluRs) are developmentally and spatially regulated throughout the hippocampus and are implicated in seizureinduced damage. In the present study we used in situ hybridization to examine possible changes in mGluR expression at the level of the hippocampus after status epilepticus in postnatal day 10 (P10) pup and adult (P40) rats. Status epilepticus did not alter expression of mGluR1, mGluR3, or mGluR5 mRNAs. In pup and adult rats, status epilepticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus. This change could lead to augmented glutamate release at mossy fiber synapses on CA3 pyramidal cells and thereby promote hyperexcitation. In pup but not adult rats, mGluR4 mRNA expression was enhanced in CA3 pyramidal neurons. Upregulation of presynaptic mGluR4 in pup CA3 neurons could lead to reduced transmitter release from CA3 axons, including recurrent collaterals, thereby reducing vulnerability of neonatal CA3 neurons to seizure-induced damage. These findings indicate that status epilepticus affects mGluR expression in a gene-and cell-specific manner, and that these changes vary with the developmental stage.

show abstract

Section: Status Epilepticus Induces Neurodegeneration In Adult But Nosupporting

confidence: 79%

Status Epilepticus-Induced Alterations in Metabotropic Glutamate Receptor Expression in Young and Adult Rats

et al. 1997

View full text Add to dashboard Cite

show abstract

“…Enhanced hippocampal plasticity likely plays a significant role in both the memory-enhancing effects of prenatal choline supplementation (Meck & Williams, 2003;McCann et al, 2006) and its neuroprotective actions. Much like our prenatal choline supplemented adult rats, juvenile rats that experience SE also show resistance to seizure-induced hippocampal cell loss, disinhibition, and mossy fiber sprouting (Sperber et al, 1991;Haas et al, 2001), and exhibit savings in spatial learning and memory (Stafstrom et al, 1993;Sarkisian et al, 1997) when compared to adult rats that experience SE. The retention of juvenile-like neuroplasticity and response to seizures into adulthood may contribute to prenatal choline supplementation's preservation of cognitive function in the face of a neural insult.…”

Section: Discussionmentioning

confidence: 99%

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

Wong-Goodrich¹,

Mellott²,

Glenn³

et al. 2008

Neurobiology of Disease

View full text Add to dashboard Cite

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...

show abstract

“…However, hilar injury, mossy fiber sprouting, and epileptogenesis do not result from SE induced in 2-week-old rat pups by either kainic acid (13) or LiPC (12,14). Because the 2-and 3-week-old pups differ in their vulnerability to LiPC SEinduced hilar injury and in the chronic development of spontaneous seizures and mossy fiber sprouting, we wondered if the observed difference may be based on differences in seizure-induced enhancement of dentate granule cell neurogenesis.…”

mentioning

confidence: 99%

Granule Cell Neurogenesis After Status Epilepticus in the Immature Rat Brain

et al. 2000

View full text Add to dashboard Cite

Summary:Purpose: Several experimental paradigms of seizure induction that produce epilepsy as a consequence have been shown to be associated with the proliferation of dentate granule cells. In developing animals, the acute sequela of hilar damage and the chronic sequelae of spontaneous seizures and mossy fiber synaptic reorganization, in response to status epilepticus, occur in an age-dependent manner. We investigated seizure-induced granule cell neurogenesis in developing rat pups to study the association between hilar injury, granule cell neurogenesis, and epilepsy.Methods: Rat pups of 2 and 3 weeks postnatal age were subjected to lithium-pilocarpine status epilepticus (LiPC SE). Rats were given bromodeoxyuridine (BrdU; 50 mglkg intraperitoneal) twice daily for 4 days beginning 3 days after SE to label dividing cells. Routine immunocytochemistry and quantification of BrdU labeling by image analysis were performed. Results were compared with previously reported data on cellular injury, mossy fiber sprouting, and spontaneous seizures in rat pups of these ages after LiPC SE.

show abstract

Resistance of the immature hippocampus to seizure-induced synaptic reorganization

Cited by 236 publications

References 43 publications

Status Epilepticus-Induced Alterations in Metabotropic Glutamate Receptor Expression in Young and Adult Rats

Status Epilepticus-Induced Alterations in Metabotropic Glutamate Receptor Expression in Young and Adult Rats

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

Granule Cell Neurogenesis After Status Epilepticus in the Immature Rat Brain

Contact Info

Product

Resources

About