Astrocytic Response in Hippocampus and Cerebral Cortex in an Experimental Epilepsy Model

Girardi, Elena; Ramos, Alberto Javier; Vanore, Gabriela; Brusco, Alicia

doi:10.1023/b:nere.0000013739.15160.a8

Cited by 20 publications

(13 citation statements)

References 39 publications

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“…The observations of the damage caused by KA (after 7 days) have been reported in our previous study [19]. KA administration (i.p.)…”

Section: Cell Morphology Following Kainate Administrationsupporting

confidence: 54%

“…However, a full development of generalized epileptic seizures was only observed in AL rats, while the extent and duration of seizures appeared attenuated in DR rats. Histopathological analysis of hippocampus region of brain in all the four groups was done as reported previously [19]. …”

Section: Administration Of Kainic Acidmentioning

confidence: 99%

“…Brain injury is known to exert a glial reaction that involves the conversion of the protoplasmic astrocytes of the gray matter into reactive astrocytes positive for glial fibrillary acidic protein (GFAP). Recent evidences suggest the robust up-regulation of GFAP after CNS insult and the levels of GFAP markedly increase during reactive gliosis when astrocytes undergo both hypertrophy and hyperplasia [19,20].…”

Section: Introductionmentioning

confidence: 99%

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Dietary Restriction Enhances Kainate-Induced Increase in NCAM While Blocking the Glial Activation in Adult Rat Brain

Sharma

Kaur

2007

Neurochem Res

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In the present study effect of dietary restriction (DR) on neuronal plasticity markers neural cell adhesion molecule (NCAM) and its polysialylated form PSA-NCAM and astrocytic marker glial fibrillary acidic protein (GFAP) was assessed following brain injury by intraperitoneal injection of kainic acid or physiological saline in adult male wistar rats. After 7-day recovery period, rats were sacrificed to study the NCAM-ir, PSA-NCAM-ir, and GFAP-ir in all the groups with immunohistofluorescence and immunoblotting. We noticed increase in NCAM and PSA-NCAM expression after KA excitotoxicity, and DR enhanced this increase in NCAM and PSA-NCAM expression. A marked increase in NCAM and PSA-NCAM-ir was observed in CA3 region of hippocampus, subgranular region and hilus of dentate gyrus, hypothalamus, and piriform cortex in both vehicle treated as well KA-treated DR rats as compared to vehicle and KA-treated AL rats, respectively. Whenever, CNS is damaged it undergoes an injury response called reactive gliosis. Our study confirmed the neuroprotective role of DR as evident from attenuation of GFAP-ir and enhanced levels of neuronal plasticity markers NCAM and PSA-NCAM. The potential beneficial role of DR regimen in attenuating KA-induced reactive astrogliosis and enhancing expression of neuronal plasticity markers may point the way to new strategies of intervention therapy by DR that will facilitate recovery from ageing and disease related neuronal dysfunction and enhance restorative processes by modulating astrogliosis.

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“…The observations of the damage caused by KA (after 7 days) have been reported in our previous study [19]. KA administration (i.p.)…”

Section: Cell Morphology Following Kainate Administrationsupporting

confidence: 54%

Section: Administration Of Kainic Acidmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Dietary Restriction Enhances Kainate-Induced Increase in NCAM While Blocking the Glial Activation in Adult Rat Brain

Sharma

Kaur

2007

Neurochem Res

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“…At MP7, NR2B expression approaching to normal values, could be losing the protective effect or could be associated with the increased astrocitic response in epileptic activity previously observed [31], considering that specific expression of NR2B subunits in astrocytes and their colocalization with R1 subunits was reported in transient global forebrain ischemia and anoxia [32].…”

Section: Discussionmentioning

confidence: 80%

The NMDAR Subunit NR2B Expression is Modified in Hippocampus after Repetitive Seizures

2008

Self Cite

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NMDA receptor is involved in synaptic plasticity, learning, memory and neurological diseases like epilepsia and it is the major mediator of excitotoxicity. NR2B-containing NMDA receptors may be playing a crucial role in epileptic disorders. In the present study the effect of the convulsant drug 3-mercaptopropionic acid (MP) repetitive administration (4-7 days) on the hippocampal NR2B subunit was studied. A significant decrease in NR2B in the whole hippocampus was observed after MP4 with a tendency to recover to normal values in MP7 by western blot assay. Immunohistochemical studies showed a decrease in several CA1 and CA2/3 strata (21-73%). MP7 showed a reversion of the drop observed at 4 days in stratum oriens, pyramidal cell layer in CA1, CA2/3 and CA1 stratum radiatum. A significant fall in the lacunosum molecular layer of both areas and stratum radiatum of CA2/3 was observed. The immunostaining in MP4 showed a decrease in the granulare layer from dentate gyrus (20%), in hillus (71%) and subicullum (63%) as compared with control and these decreases were similar at MP7 values. Results showed decreases in NR2B subunit expression in different areas following repeated MP-induce seizures, suggesting that NR2B expression is altered depending on the diverse hippocampal input and output signals of each region that could be differently involved in modulating MP-induced hyperactivity.

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“…The repetitive administration of the convulsant drug 3-mercaptopropionic acid (MP) induces tonic-clonic seizures and reactive astrogliosis in CNS (Girardi et al 2004), and the administration of the adenosine analogue cyclopentyladenosine (CPA) increases seizure threshold (Girardi et al 2007). Adenosine-a neuromodulator with endogenous anticonvulsant properties-inhibits neuronal firing and synaptic transmission acting mainly via A1 receptors, the most abundant of the four kinds of adenosine receptors described (Dunwiddie andMasino 2001, Ribeiro et al 2003), being cerebellum, a rich region in A1 receptors (Giraldez et al 1998).…”

Section: Introductionmentioning

confidence: 99%

3-Mercaptopropionic Acid-Induced Seizures Decrease NR2B Expression in Purkinje Cells: Cyclopentyladenosine Effect

et al. 2010

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Inhibitory mechanism of cerebellum epileptic activity can be involved depending on the intensity and frequency of seizure convulsions. N-methyl-D-aspartate receptors (NMDARs) play key roles in excitatory synaptic transmission and have been implicated in neurological disorders: in cerebellum, they have specific characteristics. NMDARs are heteromeric complexes, and the expression of functional receptors in mammalian cells requires the subunit NR1 (essential) and one NR2 subtype of the four isoforms: NR2A-NR2D. In mature Purkinje cells, the combination of NR1 with NR2B subunits forms functional NMDARs; NR2B subunit may be altered in exocitotoxic events. Cyclopentyladenosine (CPA), an adenosine analogue, administered to rats, for one or more days, increases seizure threshold induced by the convulsant drug 3-mercaptopropionic acid (MP). In this study, we focused on the expression of NR2B in cerebellum after repetitive seizures induced by MP and the effect of adenosine analogue CPA administered alone or previous to MP (CPA + MP). A significant decrease in NR2B in the whole cerebellum was observed after MP and CPA administration with a tendency to recover to normal values in the combined treatment of CPA administered 30 min before MP by Western blot assay. In immunohistochemical studies, NR2B expression was observed and analysed in Purkinje cells. NR2B expression was decreased after MP (55%) and CPA (12%) administration, and CPA injected 30 min before MP led to 28% reduction in Purkinje cells. These results could be related to Purkinje cell damage or alternatively to avoid the excitotoxic effect. Results recorded after CPA + MP treatment seemed involved in decreasing the convulsant MP effect.

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Astrocytic Response in Hippocampus and Cerebral Cortex in an Experimental Epilepsy Model

Cited by 20 publications

References 39 publications

Dietary Restriction Enhances Kainate-Induced Increase in NCAM While Blocking the Glial Activation in Adult Rat Brain

Dietary Restriction Enhances Kainate-Induced Increase in NCAM While Blocking the Glial Activation in Adult Rat Brain

The NMDAR Subunit NR2B Expression is Modified in Hippocampus after Repetitive Seizures

3-Mercaptopropionic Acid-Induced Seizures Decrease NR2B Expression in Purkinje Cells: Cyclopentyladenosine Effect

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