Amygdala kindling and c-fos protein(s)☆

Dragunow, Michael; Robertson, Harold A.; Robertson, G.S.

doi:10.1016/0014-4886(88)90103-3

Cited by 77 publications

(22 citation statements)

References 6 publications

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“…It is noteworthy that spontaneous seizures are the trigger for the c-fos response in our study, and these occur in the absence of anesthetic. This avoids the potential problem of underestimating the sites of activation, which sometimes occurs with this technique when animals are anesthetized (39).…”

Section: In Situ Hybridization Of C-fos Mrnamentioning

confidence: 99%

“…c-fos is a member of a multigene family coding for transcription factors, and is thought to participate in coupling neuronal excitation to changes in target gene expression (32). The induction of c-fos has previously been demonstrated in conjunction with multiple forms of seizure activity (32)(33)(34)(35)(36)(37)(38). An advantage of this approach is that it provides an overview of the sites at which intense physiologic activity has occurred.…”

Section: In Situ Hybridization Of C-fos Mrnamentioning

confidence: 99%

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Distribution and Initiation of Seizure Activity in a Rat Brain with Subcortical Band Heterotopia

et al. 2000

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Summary:Purpose: Misplaced (heterotopic) cortical neurons are a common feature of developmental epilepsies. To better understand seizure disorders associated with cortical heterotopia, the sites of aberrant discharge activity were investigated in vivo and in vitro in a seizure-prone mutant rat (tish) exhibiting subcortical band heterotopia. Methods: Depth electrode recordings and postmortem assessment of regional cfos mRNA levels were used to characterize the distribution of aberrant discharge activity during spontaneous seizures in vivo. Electrophysiologic recordings of spontaneous and evoked activity also were performed by using in vitro brain slices from the tish rat treated with proconvulsant drugs (penicillin and 4-aminopyridine). Results: Depth electrode recordings demonstrate that seizure activity begins almost simultaneously in the normotopic and heterotopic areas of the tish neocortex. Spontaneous seizures induce c-fos mRNA in normotopic and heterotopic neocortical areas, and limbic regions. The threshold concentrations of proconvulsant drugs for inducing epileptiform spiking were similar in the normotopic and heterotopic areas of tish brain slices. Manipulations that blocked communication between the norniotopic and heterotopic areas of the cortex inhibited spiking in the heterotopic, but not the normotopic, area of the cortex. Conclusions: These findings indicate that aberrant discharge activity occurs in normotopic and heterotopic areas of the neocortex, and in certain limbic regions during spontaneous seizures in the tish rat. Normotopic neurons are more prone to exhibit epileptiform activity than are heterotopic neurons in the tish cortex, and heterotopic neurons are recruited into spiking by activity initiated in normotopic neurons. The findings indicate that seizures in the tish brain primarily involve telencephalic structures, and suggest that normotopic neurons are responsible for initiating seizures in the dysplastic neocortex.

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Section: In Situ Hybridization Of C-fos Mrnamentioning

confidence: 99%

Section: In Situ Hybridization Of C-fos Mrnamentioning

confidence: 99%

Distribution and Initiation of Seizure Activity in a Rat Brain with Subcortical Band Heterotopia

et al. 2000

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“…In vivo stimulation, such as chemically and electrically induced seizures, triggers both the generation of PAF (20) and the accumulation of c-fos mRNA (21)(22)(23)(24) and zif-268 mRNA (25,26) in the brain. Intracerebroventricular injection of BN-50730 prior to stimulation partially inhibits the c-fos message accumulation and markedly inhibits zif-268 expression (19), suggesting that PAF is an intracellular messenger that activates gene expression through a BN-50730 sensitive intracellular PAF receptor.…”

mentioning

confidence: 99%

“…The TISJO/PGS-2 primary response gene was identified as one of several phorbol ester (28) and serum (29) inducible genes in NIH 3T3 cells, and as a v-src-inducible gene in chicken embryo fibroblasts (30 [20][21][22][23][24][25][26][27][28][29][30] pl of the supernatant after normalization of -3-galactosidase, was used in each assay and was mixed with 70-80 /4 of 2x ALL buffer. The reaction was initiated by the injection of 100 gl of 1 mM luciferin and the relative light units were determined by using an ALL luminometer recording over a 20-sec interval.…”

mentioning

confidence: 99%

Platelet-activating factor and retinoic acid synergistically activate the inducible prostaglandin synthase gene.

Bazán

Fletcher

Herschman

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

139

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Platelet-activating factor (PAF), a potent lipid mediator generated in cell injury and in the inflammatory and immune responses, promotes transcriptional activation of several primary response genes. TIS10/PGS-2 is a primary response gene encoding the inducible form of prostaglandin synthase. The inductive effects of PAF and retinoic acid (RA), alone and in combination, were studied with the regulatory region of TIS10/PGS-2 transfected into an exponentially growing glioblastoma-neuroblastoma NG108-15 hybrid in the human SH-SY5Y neuroblastoma or in the NIH 3T3 cell. RA alone exhibited only a small inductive effect. However, in the presence of RA (100 nM), a PAF-dependent (1-50 nM) synergistic activation of luciferase reporter constructs driven by regulatory regions of the TIS10/PGS-2 gene was found. The hetrazepine BN-50730, an antagonist selective for intracellular PAF binding sites, inhibited PAF and RA induction of luciferase from the TIS10/PGS-2 promoter. Thus, the intracellular PAF binding site is involved in TIS10/PGS-2 expression. Induction is rapid, suggesting that the combination of PAF and RA activates a preexisting latent transcription factor(s). Deletion studies restrict the major PAF and RA cis-acting response element of the TIS10/PGS-2 gene to a 70-nucleotide sequence as an intracellular inducer of TIS10/PGS-2 expression. The synergistic effect of RA and PAF represents an unusual convergence of nuclear signaling pathways by which, through the modulation of preexisting transcription factors, specific gene expression can be upregulated. PAF-dependent induction of TIS10/PGS-2 expression may play a role in cell injury, differentiation, inflammation, and immune responses.

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“…Perhaps one of the best characterized such circuit is the entorhinal-hippocampal-entorhinal network , which facilitates the flow of signals via the following neuronal connections: layer II of the entorhinal cortex → granule cell layer of the dentate gyrus → CA3 → CA2 → CA1 → subiculum → layers V-VI of the entorhinal cortex → layer II of the entorhinal cortex (Witter et al, 1989). Activation of this circuit by seizures has been reported in other models of MTLE, such as the systemic kainic acid (Popovici et al, 1990) and pilocarpine models (Harvey and Sloviter, 2005) and in models of amygdala kinding (Dragunow et al, 1988). Depth electrode EEG recordings from patients with MTLE also suggest that this circuit is preferentially involved during seizures (Spencer and Spencer, 1994).…”

Section: Discussionmentioning

confidence: 84%

Progressive neuronal activation accompanies epileptogenesis caused by hippocampal glutamine synthetase inhibition

Albright

Dhaher

Wang

et al. 2017

Experimental Neurology

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Loss of glutamine synthetase (GS) in hippocampal astrocytes has been implicated in the causation of human mesial temporal lobe epilepsy (MTLE). However, the mechanism by which the deficiency in GS leads to epilepsy is incompletely understood. Here we ask how hippocampal GS inhibition affects seizure phenotype and neuronal activation during epilepsy development (epileptogenesis). Epileptogenesis was induced by infusing the irreversible GS blocker methionine sulfoximine (MSO) unilaterally into the hippocampal formation of rats. We then used continuous video-intracranial electroencephalogram (EEG) monitoring and c-Fos immunohistochemistry to determine the type of seizures and spatial distribution of neuronal activation early (1–5 days postinfusion) and late (16–43 days postinfusion) in epileptogenesis. Early in epileptogenesis, seizures were preferentially mild (stage 1–2), activating neurons in the entorhinal-hippocampal area, the basolateral amygdala, the piriform cortex, the midline thalamus, and the anterior olfactory area. Late in epileptogenesis, the seizures were generally more severe (stage 4–5) with neuronal activation extending to the neocortex, the bed nucleus of the stria terminalis, the mediodorsal thalamus, and the central nucleus of the amygdala. Our findings demonstrate that inhibition of GS focally in the hippocampal formation triggers a process of epileptogenesis characterized by gradual worsening of seizure severity and involvement of progressively larger neuronal populations over a period of several weeks. Knowledge about the underlying mechanism of epileptogenesis is important because such knowledge may result in more specific and efficacious treatments of MTLE by moving away from large and poorly specific surgical resections to highly targeted surgical or pharmacological interventions of the epileptogenic process.

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Amygdala kindling and c-fos protein(s)☆

Cited by 77 publications

References 6 publications

Distribution and Initiation of Seizure Activity in a Rat Brain with Subcortical Band Heterotopia

Distribution and Initiation of Seizure Activity in a Rat Brain with Subcortical Band Heterotopia

Platelet-activating factor and retinoic acid synergistically activate the inducible prostaglandin synthase gene.

Progressive neuronal activation accompanies epileptogenesis caused by hippocampal glutamine synthetase inhibition

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