Differential Expression of S100β and Glial Fibrillary Acidic Protein in the Hippocampus after Kainic Acid-Induced Lesions and Mossy Fiber Sprouting in Adult Rat

Bendotti, Caterina; Guglielmetti, Filippo; Tortarolo, Massimo; Samanin, R.; Hirst, Warren D.

doi:10.1006/exnr.1999.7262

Cited by 33 publications

(26 citation statements)

References 36 publications

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“…Further work is required to establish the role of activated microglial cells in neurodegeneration and/or epileptogenesis in our model. Our findings regarding astrogliosis are in partial agreement with other studies, where GFAP immunoreactivity steadily increased from Days 1 to 3 up to one month following intrahippocampal (Bendotti et al 2000) or i.p. (Ding et al 2000) KA administration.…”

Section: Discussionsupporting

confidence: 93%

Temporal Profile of Clinical Signs and Histopathologic Changes in an F-344 Rat Model of Kainic Acid–induced Mesial Temporal Lobe Epilepsy

et al. 2008

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Since there is limited information in the literature, the purpose of this study was to investigate clinical signs, morphology, and temporal progression of lesions from Days 3 to 168 in a kainic acid (KA)-induced Fischer-344 (F-344) rat model of mesial temporal lobe epilepsy (MTLE). Following a single KA subcutaneous dose of 9 mg/kg to young adult male rats, 95% survived, 93% exhibited status epilepticus, and 80% eventually developed spontaneous motor seizures. Histopathology included hematoxylin and eosin (H&E), autofluorescence, Fluoro-Jade B, Timm's, ED-1/CD68, GFAP, doublecortin, and Ki-67. Neuronal degeneration occurred on Day 3 in the hippocampal CA1, CA3, and dentate hilar regions; amygdaloid and thalamic nuclei; and frontoparietotemporal, entorhinal and piriform cortices. Degeneration severity peaked on Day 6 and decreased progressively until Day 168. Aberrant mossy fiber (MF) sprouting was present in the inner molecular layer of dentate gyrus on Days 6-168. Microliosis and astrogliosis peaked on Day 28 and generally colocalized with the distribution of neuronal degeneration. Important correlates to human MTLE included induction of spontaneous seizures, more severe neuronal damage of CA1 than CA3 (in contrast to other animal models but similar to humans), hilar neuronal loss, activated microgliosis and astrogliosis, aberrant MF sprouting, and dentate granule cell neurogenesis. Aberrant MF sprouting prior to spontaneous motor seizures and reduced seizure frequency with a decrease in aberrant MF sprouting support the hypothesis that MF sprouts are necessary for spontaneous seizure generation and maintenance.

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Section: Discussionsupporting

confidence: 93%

Temporal Profile of Clinical Signs and Histopathologic Changes in an F-344 Rat Model of Kainic Acid–induced Mesial Temporal Lobe Epilepsy

et al. 2008

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“…Similar to our results, other studies have also found significant increases in GFAP gene expression in both the latent and chronic stages of epilepsy (Lukasiuk and Pitkänen, 2004). Our findings also match previous studies that demonstrated increased GFAP expression in the electrical kindling (Miyazaki et al, 2003; Stringer, 1996; Torre et al, 1993), pentylenetetrazol (PTZ) (Torre et al, 1993), kainic acid (Bendotti et al, 2000; Lee et al, 2012b), and frequent repetitive febrile seizures (FRFS) (Yang et al, 2009) models of epilepsy.…”

Section: Discussionsupporting

confidence: 91%

Regulation of astrocyte glutamate transporter-1 (GLT1) and aquaporin-4 (AQP4) expression in a model of epilepsy

Hubbard

Szu

Yonan

et al. 2016

Experimental Neurology

118

106

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Astrocytes regulate extracellular glutamate and water homeostasis through the astrocyte-specific membrane proteins glutamate transporter-1 (GLT1) and aquaporin-4 (AQP4), respectively. The role of astrocytes and the regulation of GLT1 and AQP4 in epilepsy are not fully understood. In this study, we investigated the expression of GLT1 and AQP4 in the intrahippocampal kainic acid (IHKA) model of temporal lobe epilepsy (TLE). We used real-time polymerase chain reaction (RT-PCR), Western blot, and immunohistochemical analysis at 1, 4, 7, and 30 days after kainic acid-induced status epilepticus (SE) to determine hippocampal glial fibrillary acidic protein (GFAP, a marker for reactive astrocytes), GLT1, and AQP4 expression changes during the development of epilepsy (epileptogenesis). Following IHKA, all mice had SE and progressive increases in GFAP immunoreactivity and GFAP protein expression out to 30 days post-SE. A significant initial increase in dorsal hippocampal GLT1 immunoreactivity and protein levels were observed 1 day post SE and followed by a marked downregulation at 4 and 7 days post SE with a return to near control levels by 30 days post SE. AQP4 dorsal hippocampal protein expression was significantly downregulated at 1 day post SE and was followed by a gradual return to baseline levels with a significant increase in ipsilateral protein levels by 30 days post SE. Transient increases in GFAP and AQP4 mRNA were also observed. Our findings suggest that specific molecular changes in astrocyte glutamate transporters and water channels occur during epileptogenesis in this model, and suggest the novel therapeutic strategy of restoring glutamate and water homeostasis.

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“…We found no apoptotic cell death in the 6-monthold NC lox/lox Cre mouse brain (data not shown), suggesting that the epileptic seizure observed in NC lox/lox Cre mice was not attributable to the neurodegeneration. Morphological alteration of the hippocampus is a prominent example of epileptic seizure, because it is observed in animal models of epilepsy and also in human epileptic patients (18,19,20). Immunostaining with anti-doublecortin polyclonal antibody revealed that newborn neuroblasts generated from the subgranular zone of dentate gyrus were rather increased in the epileptic NC lox/lox Cre mouse (Fig.…”

Section: Generation and Basic Characterization Of The Mutant Mice-mentioning

confidence: 95%

“…Under a high power field microscope, both GFAP-and S100␤-expressing cells clearly showed hypertrophic profiles with the thick processes from the large cell body when compared with NC lox/wt Cre mice. Astrocytes play a major support role for a wide range of neural processes, including neural growth and sprouting, and are observed to be activated in the process of epileptogenesis (18,19,20). Taken together, these age-dependent phenotypes are related at least to the progressive neurochondrin deficiency by neural cell turnover, although some other pathophysiological factor possibly affecting the rate of incidence is still unclear.…”

Section: Generation and Basic Characterization Of The Mutant Mice-mentioning

confidence: 99%

Neurochondrin Negatively Regulates CaMKII Phosphorylation, and Nervous System-specific Gene Disruption Results in Epileptic Seizure

Dateki

Horii

Kasuya

et al. 2005

Journal of Biological Chemistry

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Neurochondrin is a novel cytoplasmic protein and possibly involved in neurite outgrowth, chondrocyte differentiation, and bone metabolism. Our previous trial in disclosing its role by the loss of function in mice failed because of the lethality in utero. In this study, we eliminated the neurochondrin gene expression preferentially in the nervous system by the conditional knockout strategy. Our results showed that neurochondrin is a negative regulator of Ca 2؉ /calmodulin-dependent protein kinase II phosphorylation and essential for the spatial learning process but not for the differentiation or neurite outgrowth of the neuron. In addition, the nervous system-specific homozygous gene disruption resulted in epileptic seizure.

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Differential Expression of S100β and Glial Fibrillary Acidic Protein in the Hippocampus after Kainic Acid-Induced Lesions and Mossy Fiber Sprouting in Adult Rat

Cited by 33 publications

References 36 publications

Temporal Profile of Clinical Signs and Histopathologic Changes in an F-344 Rat Model of Kainic Acid–induced Mesial Temporal Lobe Epilepsy

Temporal Profile of Clinical Signs and Histopathologic Changes in an F-344 Rat Model of Kainic Acid–induced Mesial Temporal Lobe Epilepsy

Regulation of astrocyte glutamate transporter-1 (GLT1) and aquaporin-4 (AQP4) expression in a model of epilepsy

Neurochondrin Negatively Regulates CaMKII Phosphorylation, and Nervous System-specific Gene Disruption Results in Epileptic Seizure

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