Functional mapping of limbic seizures originating in the hippocampus: a combined 2-deoxyglucose and electrophysiologic study

Lothman, Eric W.; Hatlelid, J. M.; Zorumski, Charles F.

doi:10.1016/0006-8993(85)91224-7

Cited by 97 publications

(31 citation statements)

References 21 publications

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“…In addition, GFAP mRNA was increased throughout the hippocampus and dentate gyrus. This is consistent with the known pattern of seizure activity that occurs in kindled animals, where kindled seizures occur bilaterally and involve both the hippocampus proper and the dentate gyrus (10). This pattern of increased GFAP mRNA was observed in all three animals that were evaluated after having received multiple seizures (12 per day every other day) for 25-30 days.…”

supporting

confidence: 68%

Neuronal activity up-regulates astroglial gene expression.

Steward

Torre

Tomasulo

et al. 1991

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

170

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supporting

confidence: 68%

Neuronal activity up-regulates astroglial gene expression.

Steward

Torre

Tomasulo

et al. 1991

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

170

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“…Whether the late (1 month) reduction in somatostatin-LI release efficacy in the hippocampus is prodromic to cell death remains to be established. Furthermore, the late increase in somatostatin-LI release in the cortex and the transient elevation found in the striatum indicate that somatostatin neurons are differentially affected in extralimbic regions that are likely to be recruited in the kindling circuit (Lothman et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Time‐ and Region‐Specific Variations in Somatostatin Release Following Amygdala Kindling in the Rat

Simonato

Bregola

Beani

et al. 1998

Journal of Neurochemistry

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Somatostatin biosynthesis is activated during and following kindling epileptogenesis. The aim of this study was to investigate whether this phenomenon translates into enhanced release of the peptide and whether it is involved in kindling maintenance. A marked increase in somatostatin-like immunoreactivity (somatostatin-LI) was observed in hilar interneurons of the hippocampus and in their presumed projections to the outer molecular layer 1 week, but not 1 month, after the last kindled seizure. No overt changes were observed in the striatum or in the cortex. Compared with sham-stimulated controls, (a) in the hippocampus, high-K~-evokedsomatostatin-LI release was unchanged in synaptosomes taken from rats killed 7 days after the last kindled seizure but was bilaterally reduced after 30 days; (b) in the striatum, it was increased (mainly ipsilaterally to stimulation) 7, but not 30, days after the last seizure; and (c) in the cortex, somatostatin-LI release was bilaterally increased in synaptosomes taken from kindled rats 30, but not 7, days after the last seizure. This study shows that distinct changes occur in synaptosomal somatostatin-LI release after kindling acquisition, depending on the brain area analyzed and on the time elapsed from the last generalized seizure.

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“…Seizure grades 1–2 are classified as forebrain seizures since these seizures are clonic and require forebrain structures for their expression (Engel, et al, 1978, Ferland, et al, 1998, Lothman, et al, 1985, Namba, et al, 1991, Samoriski and Applegate, 1997, Samoriski, et al, 1997). Grades 3–7 denote a seizure type that begins as a clonic-forebrain seizure where the animal losses its postural control, regains its posture, and rapidly progresses into a brainstem seizure (we refer to such seizures as forebrain→brainstem seizures to denote the seizure progression of this type).…”

Section: Methodsmentioning

confidence: 99%

Spatiotemporal differences in the c-fos pathway between C57BL/6J and DBA/2J mice following flurothyl-induced seizures: A dissociation of hippocampal Fos from seizure activity

et al. 2015

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Significant differences in seizure characteristics between inbred mouse strains highlight the importance of genetic predisposition to epilepsy. Here, we examined the genetic differences between the seizure-resistant C57BL/6J (B6) mouse strain and the seizure-susceptible DBA/2J (D2) strain in the phospho-Erk and Fos pathways to examine seizure-induced neuronal activity to uncover potential mechanistic correlates to these disparate seizure responsivities. Expression of neural activity markers was examined following 1, 5, or 8 seizures, or after 8 seizures, a 28 day rest period, and a final flurothyl rechallenge. Two brain regions, the hippocampus and ventromedial nucleus of the hypothalamus (VMH), had significantly different Fos expression profiles following seizures. Fos expression was highly robust in B6 hippocampus following one seizure and remained elevated following multiple seizures. Conversely, there was an absence of Fos (and phospho-Erk) expression in D2 hippocampus following one generalized seizure that increased with multiple seizures. This lack of Fos expression occurred despite intracranial electroencephalographic recordings indicating that the D2 hippocampus propagated ictal discharge during the first flurothyl seizure suggesting a dissociation of seizure discharge from Fos and phospho-Erk expression. Global transcriptional analysis confirmed a dysregulation of the c-fos pathway in D2 mice following 1 seizure. Moreover, global analysis of RNA expression differences between B6 and D2 hippocampus revealed a unique pattern of transcripts that were co-regulated with Fos in D2 hippocampus following 1 seizure. These expression differences could, in part, account for D2’s seizure susceptibility phenotype. Following 8 seizures, a 28 day rest period, and a final flurothyl rechallenge, ~85% of B6 mice develop a more complex seizure phenotype consisting of a clonic-forebrain seizure that uninterruptedly progresses into a brainstem seizure. This seizure phenotype in B6 mice is highly correlated with bilateral Fos expression in the VMH and was not observed in D2 mice, which always express clonic-forebrain seizures upon flurothyl retest. Overall, these results illustrate specific differences in protein and RNA expression in different inbred strains following seizures that precede the reorganizational events that affect seizure susceptibility and changes in seizure semiology over time.

show abstract

Functional mapping of limbic seizures originating in the hippocampus: a combined 2-deoxyglucose and electrophysiologic study

Cited by 97 publications

References 21 publications

Neuronal activity up-regulates astroglial gene expression.

Neuronal activity up-regulates astroglial gene expression.

Time‐ and Region‐Specific Variations in Somatostatin Release Following Amygdala Kindling in the Rat

Spatiotemporal differences in the c-fos pathway between C57BL/6J and DBA/2J mice following flurothyl-induced seizures: A dissociation of hippocampal Fos from seizure activity

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