The grafted hippocampus: An epileptic focus
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Cited by (38)
From treatment to cure: Stopping seizures, preventing seizures, and reducing brain propensity to seize
2014, International Review of NeurobiologyStem cells as a potential therapy for epilepsy
2013, Experimental NeurologyCitation Excerpt :This makes the overall phenotype of the transplanted cells uncertain. Another cautionary tale was provided by an early transplant study from Buzsaki et al. (1989). They transplanted solid blocks of fetal rat hippocampus (E15–16) into adult rat hippocampi that had undergone disruption of the fimbria/fornix, the primary conduit for subcortical efferent and afferent fibers for the hippocampus.
Modeling epilepsy with pluripotent human cells
2009, Epilepsy and BehaviorCell and gene therapies in epilepsy - promising avenues or blind alleys?
2008, Trends in NeurosciencesCitation Excerpt :It was therefore important to study whether transplantation of fetal cells to a damaged hippocampus in such models would also provide antiepileptogenic or anticonvulsant effects as observed in the kindling model. Furthermore, such evaluation of hippocampal fetal cell grafts on chronic seizures in rat models of TLE is crucial for potential clinical application of this approach because some studies reported that grafts themselves might generate seizures under certain conditions [17–19]. In the kainate model of TLE, transplantation of hippocampal or locus coeruleus neurons to the ventricles or hippocampus of rats after a kainate-induced SE significantly reduced the frequency of spontaneous seizures compared to sham controls [20].
Cell therapy in models for temporal lobe epilepsy
2007, SeizureCitation Excerpt :Spontaneous EEG seizures were also frequently recorded from the graft which spread into the host brain.35,36 Moreover, spontaneous behavioural convulsions were detected in a high fraction of the transplanted rats.34,37,39 Although the exact mechanism for this transplantation-induced epileptiform activity was not unravelled, the authors suggested that the hyperexcitability of the graft was caused by a lack of afferent control, extensive formation of recurrent excitatory circuitry and insufficient GABAergic inhibition within the graft.37