Does Acquired Epileptogenesis in the Immature Brain Require Neuronal Death?

Baram, Tallie Z.; Jensen, Frances E.; Brooks‐Kayal, Amy R.

doi:10.5698/1535-7511-11.1.21

Cited by 33 publications

(30 citation statements)

References 82 publications

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“…It was documented that neuronal loss occurred in some neonatal seizure models, though in other animal models, such as hypoxia-induced model cell loss, it might not occur (Koh et al, 2004;Bjorkman et al, 2010;Dunleavy et al, 2010;Baram et al, 2011;Wang et al, 2011). Therefore, hypoxia-induced neonatal seizures may be not sufficient to induce hippocampal damage.…”

Section: Effects Of Hypoxia-induced Neonatal Seizures On Mfs and Neurmentioning

confidence: 94%

In vivo effects of bumetanide at brain concentrations incompatible with NKCC1 inhibition on newborn DGC structure and spontaneous EEG seizures following hypoxia-induced neonatal seizures

Wang¹,

Zhang²,

Song³

et al. 2015

Neuroscience

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Section: Effects Of Hypoxia-induced Neonatal Seizures On Mfs and Neurmentioning

confidence: 94%

In vivo effects of bumetanide at brain concentrations incompatible with NKCC1 inhibition on newborn DGC structure and spontaneous EEG seizures following hypoxia-induced neonatal seizures

Wang¹,

Zhang²,

Song³

et al. 2015

Neuroscience

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“…However, repeated seizures cause neuronal injury and cell death depending on a number of variables such as the age of the animal, seizure type and duration [19] . For example, in the immature brain, recurrent seizures cause very little neuronal injury, and cell loss is not required for the development of epilepsy late in life [20][21][22][23] .…”

Section: Association Of Post-se Epilepsy With Mossy Fiber Sprouting Vmentioning

confidence: 99%

One hour of pilocarpine-induced status epilepticus is sufficient to develop chronic epilepsy in mice, and is associated with mossy fiber sprouting but not neuronal death

et al. 2013

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Determining the minimal duration of status epilepticus (SE) that leads to the development of subsequent spontaneous seizures (i.e., epilepsy) is important, because it provides a critical time-window for seizure intervention and epilepsy prevention. In the present study, male ICR (Imprinting Control Region) mice were injected with pilocarpine to induce acute seizures. SE was terminated by diazepam at 10 min, 30 min, 1 h, 2 h and 4 h after seizure onset. Spontaneous seizures occurred in the 1, 2 and 4 h SE groups, and the seizure frequency increased with the prolongation of SE. Similarly, the Morris water maze revealed that the escape latency was significantly increased and the number of target quadrant crossings was markedly decreased in the 1, 2 and 4 h SE groups. Robust mossy fiber sprouting was observed in these groups, but not in the 10 or 30 min group. In contrast, Fluoro-Jade B staining revealed significant cell death only in the 4 h SE group. The incidence and frequency of spontaneous seizures were correlated with Timm score (P = 0.004) and escape latency (P = 0.004). These data suggest that SE longer than one hour results in spontaneous motor seizures and memory deficits, and spontaneous seizures are likely associated with robust mossy fiber sprouting but not neuronal death.

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“…However, the majority of evidence suggests that even prolonged seizures and SE are less likely to provoke cell death during development (70,71,(97)(98)(99)(100)(101)(102). Reorganization of neuronal connectivity is another common outcome of seizures in the mature brain.…”

Section: Excitotoxicity Throughout the Life Cyclementioning

confidence: 99%

The Brain, Seizures and Epilepsy Throughout Life: Understanding a Moving Target

Baram

2012

Epilepsy Curr

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The Scope of the Problem The incidence of seizures and of epilepsy varies throughout life, peaking in neonates and children and increasing again after the age of 50 (1-4). In addition to the quantitative measure of the incidence of seizures, the type of seizures (and of epilepsy syndromes) varies with age: for example, febrile seizures take place in infants and children (1, 5-7), whereas the incidence of post-stroke epilepsy increases in adults compared with children (1,3,8). What is the basis of these age-dependent variations? What are the age-specific properties of the brain that contribute to the probability of seizure generation and to the nature of the resulting seizure?A second, reciprocal aspect of the interaction of the age of the brain and seizures involves the effects of a seizure on the structure and function of neurons and neuronal networks. Here, again, clinical evidence suggests that the consequences of a seizure might vary with age. For example, the consequences of status epilepticus (SE) in young children seem to depend on the inciting etiology (9, 10), and, in general, mortality and cognitive outcomes are more favorable than in the adult and elderly individual (11)(12)(13)(14). In contrast, status epilepticus in adult and aging individuals can have major detrimental effects on cognitive function and even survival (14-16). What is the basis of these age-dependent variations? What are the age-specific properties of the brain that modulate the effects of seizures on neuronal integrity and function?These questions are of paramount clinical importance because they should provide clues for developing age-specific diagnostic tools, prognostic models, and intervention strategies. Thus, while the answers to these questions are not fully elucidated, the questions provide a framework for discussing the salient elements of the evolving interaction between the brain and seizures throughout life.The following paragraphs highlight a few of the many facts that influence age-specific seizures and the age-specific consequences of seizures. Because most of the direct information about seizures throughout the life-span often derives from animal models, these are discussed. The author regrets that this overview is not comprehensive and likely omits a number of important publications. Nonetheless, this review serves to illustrate crucial features of the topic. Age-Specific Brain Properties Influence Seizures That Are Generated During Each AgeWhereas brain development from embryonic life to senescence is a continuum, here it is divided into four stages: the neonatal, childhood, adulthood, and aging epochs. The Neonatal Brain and Age-Specific Neonatal SeizuresThe neonatal brain is in a stage of rapid flux from both structural and functional perspectives. Neurons are still being born, circuits are being formed, and synapses are being established (17,18). Synaptic currents are often slower (19), neurotransmitters play trophic roles (20), and circuits are not fully mature (21). These facts predict that seizures may propag...

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Does Acquired Epileptogenesis in the Immature Brain Require Neuronal Death?

Cited by 33 publications

References 82 publications

In vivo effects of bumetanide at brain concentrations incompatible with NKCC1 inhibition on newborn DGC structure and spontaneous EEG seizures following hypoxia-induced neonatal seizures

In vivo effects of bumetanide at brain concentrations incompatible with NKCC1 inhibition on newborn DGC structure and spontaneous EEG seizures following hypoxia-induced neonatal seizures

One hour of pilocarpine-induced status epilepticus is sufficient to develop chronic epilepsy in mice, and is associated with mossy fiber sprouting but not neuronal death

The Brain, Seizures and Epilepsy Throughout Life: Understanding a Moving Target

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