Anticonvulsant action and long-term effects of gabapentin in the immature brain

Cilio, Maria Roberta; Bolanos, Addison; Liu, Z; Schmid, Regula; Yang, Yili; Stafstrom, Carl E.; Mikati, Mohamad A.; Holmes, Gregory L.

doi:10.1016/s0028-3908(00)00103-9

Cited by 77 publications

(44 citation statements)

References 28 publications

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“…Experiments were performed according to Mikati et al (2001) and Cilio et al (2001). Briefly, a circular tank (200 cm diameter) was filled with opaque water (22 Ϯ 1°C), and a wooden platform (10 ϫ 10 cm) was positioned in the center of one quadrant of the pool 2.5 cm below the water surface.…”

Section: Methodsmentioning

confidence: 99%

“…Rats were perfused with 4% paraformaldehyde, and coronal sections throughout the dorsal hippocampus were processed in serial order for immunohistochemistry with mouse anti-neuronal-specific nuclear protein (NeuN) monoclonal antibody (1:500 dilution; Chemicon, Temecula, CA). Neuronal damage was scored in areas CA1 and CA3 of the hippocampus according to the following scale (Bozzi et al, 2000;Cilio et al, 2001): 0, no damage; 1, minimal damage (small spots of degeneration); 2, evident loss of pyramidal neurons; 3, complete disruption of hippocampal architecture. An average number of 10 sections per animal were analyzed by an investigator unaware of the treatment.…”

Section: Methodsmentioning

confidence: 99%

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Antiepileptic Effects of Botulinum Neurotoxin E

Costantin¹,

Bozzi²,

Richichi³

et al. 2005

J. Neurosci.

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Experimental studies suggest that the delivery of antiepileptic agents into the seizure focus might be of potential utility for the treatment of focal-onset epilepsies. Botulinum neurotoxin E (BoNT/E) causes a prolonged inhibition of neurotransmitter release after its specific cleavage of the synaptic protein synaptosomal-associated protein of 25 kDa (SNAP-25). Here, we show that BoNT/E injected into the rat hippocampus inhibits glutamate release and blocks spike activity of pyramidal neurons. BoNT/E effects persist for at least 3 weeks, as determined by immunodetection of cleaved SNAP-25 and loss of intact SNAP-25. The delivery of BoNT/E to the rat hippocampus dramatically reduces both focal and generalized kainic acid-induced seizures as documented by behavioral and electrographic analysis. BoNT/E treatment also prevents neuronal loss and long-term cognitive deficits associated with kainic acid seizures. Moreover, BoNT/Einjected rats require 50% more electrical stimulations to reach stage 5 of kindling, thus indicating a delayed epileptogenesis. We conclude that BoNT/E delivery to the hippocampus is both antiictal and antiepileptogenic in experimental models of epilepsy.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Antiepileptic Effects of Botulinum Neurotoxin E

Costantin¹,

Bozzi²,

Richichi³

et al. 2005

J. Neurosci.

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“…A study shows that young (postnatal day 35) animals treated with GBP for 40 days following the KA-induced SE exhibited reduced incidence of SRMS, a better pathology score, diminished aggressiveness, and no long-term adverse consequences on cognitive processes (Cilio et al, 2001). Thus, this drug has some promise but detailed investigations on its anti-epileptogenic neuroprotective properties are needed.…”

Section: Gabapentin-gabapentin (Gbp)mentioning

confidence: 99%

Progress in neuroprotective strategies for preventing epilepsy

Acharya

Hattiangady

Shetty

2008

Progress in Neurobiology

157

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Neuroprotection is increasingly considered as a promising therapy for preventing and treating temporal lobe epilepsy (TLE). The development of chronic TLE, also termed as epileptogenesis, is a dynamic process. An initial precipitating injury (IPI) such as the status epilepticus (SE) leads to neurodegeneration, abnormal reorganization of the brain circuitry and a significant loss of functional inhibition. All of these changes likely contribute to the development of chronic epilepsy, characterized by spontaneous recurrent motor seizures (SRMS) and learning and memory deficits. The purpose of this review is to discuss the current state of knowledge pertaining to neuroprotection in epileptic conditions, and to highlight the efficacy of distinct neuroprotective strategies for preventing or treating chronic TLE. Although the administration of certain conventional and new generation antiepileptic drugs is effective for primary neuroprotection such as reduced neurodegeneration after acute seizures or the SE, their competence for preventing the development of chronic epilepsy after an IPI is either unknown or not promising. On the other hand, alternative strategies such as the ketogenic diet therapy, administration of distinct neurotrophic factors, hormones or antioxidants seem useful for preventing and treating chronic TLE. However, long term studies on the efficacy of these approaches introduced at different time-points after the SE or an IPI are lacking. Additionally, grafting of fetal hippocampal cells at early time-points after an IPI holds considerable promise for preventing TLE, though issues regarding availability of donor cells, ethical concerns, timing of grafting after SE, and durability of graft-mediated seizure suppression need to be resolved for further advances with this approach. Overall, from the studies performed so far, there is consensus that neuroprotective strategies need to be employed as quickly as possible after the onset of the SE or an IPI for considerable beneficial effects. Nevertheless, ideal strategies that are capable of facilitating repair and functional recovery of the brain after an IPI and preventing the evolution of IPI into chronic epilepsy are still hard to pin down.

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“…Thus, most potential neuroprotective agents have targeted excitotoxic pathways, including blockade of glutaminergic NMDA receptors and calcium channels [70][71][72][73][74][75], or, alternatively, apoptotic pathways [76]. A number of AEDs have also been shown to have potential neuroprotective properties, chiefly valproate and topiramate [77][78][79][80][81][82][83][84][85][86][87]. The data on these agents come from various animal models of SE.…”

Section: Neuroprotection In Status Epilepticusmentioning

confidence: 99%

Status epilepticus: a modern approach to management

Kinirons

Doherty²

2008

European Journal of Emergency Medicine

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Status epilepticus (SE) is a common medical emergency. Two problems continue to militate against improved outcome in SE, namely, failure to recognize the wide spectrum of clinical presentation and failure to treat in an appropriately aggressive and timely manner. In this study, we aim to provide a clear understanding of the clinical presentation of SE, as well as providing an evidence-based review of the pathophysiological consequences of prolonged seizures, enabling the reader to adopt a rational approach to its management. We discuss current best practice for the management of SE as well as discussing alternative strategies, and briefly explore possible future therapeutic interventions.

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Anticonvulsant action and long-term effects of gabapentin in the immature brain

Cited by 77 publications

References 28 publications

Antiepileptic Effects of Botulinum Neurotoxin E

Antiepileptic Effects of Botulinum Neurotoxin E

Progress in neuroprotective strategies for preventing epilepsy

Status epilepticus: a modern approach to management

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