Altered short-term plasticity in the prefrontal cortex after early life seizures

Hernan, Amanda E.; Holmes, Gregory L.; Isaev, Dmytro; Scott, Rod C.; Isaeva, Elena

doi:10.1016/j.nbd.2012.10.007

Cited by 39 publications

(33 citation statements)

References 69 publications

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“…This hypothesis has also been tested in rodents. Recurrent flurothyl seizures induced during the neonatal period lead to an increase in LTP in the somatosensory cortex and to increases in STP in the prefrontal cortex (Isaeva et al 2010;Hernan et al 2013). Similar effects on plasticity have also been identified following postnatal hypoxic seizures (Jensen 1999;Zhou et al 2011).…”

Section: The Impact Of Seizuresmentioning

confidence: 74%

Mechanisms Responsible for Cognitive Impairment in Epilepsy

Lenck-Santini

Scott

2015

Cold Spring Harb Perspect Med

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Epilepsy is often associated with cognitive and behavioral impairments that can have profound impact on the quality of life of patients. Although the mechanisms of cognitive impairment are not completely understood, we make an attempt to describe, from a systems perspective, how information processing is affected in epilepsy disorders. The aim of this review is to (1) define the nature of cognitive deficits associated with epilepsy, (2) review fundamental systems-level mechanisms underlying information processing, and (3) describe how information processing is dysfunctional in epilepsy and investigate the relative contributions of etiology, seizures, and interictal discharges (IDs). We conclude that these mechanisms are likely to be important and deserve more detailed scrutiny in the future.T he epilepsies are a group of disorders defined by the propensity for an individual to have epileptic seizures (Fisher et al. 2014). In addition to seizures, these common and serious neurological disorders are associated with cognitive and behavioral impairments (Berg and Scheffer 2011). The cognitive and behavioral impairments are critical determinants of the reductions in quality of life observed in patients with epilepsy (Ronen et al. 2003;Loring et al. 2004). It is, therefore, of major importance that the mechanisms underlying cognitive impairments are characterized as this is likely to lead to novel interventions that will ultimately improve the quality of life of people with epilepsy. Epilepsy is associated with a variety of physiological and molecular alterations at the level of changes in the genome, gene expression, receptor characteristics, peptides, and brain injury. These changes are not only responsible for seizures but also for functional abnormalities underlying cognitive impairment. It is likely that several of these mechanisms are occurring in concert, and, therefore, it is important to study the net effects of these alterations at the level of neural networks as this may also lead to novel interventions that could improve outcomes. The aims of this article are to (1) define the nature of cognitive deficits associated with epilepsy, (2) review fundamental systems-level mechanisms underlying information processing, and (3) describe how information processing is dysfunctional in epilepsy and investigate the relative contributions of etiology, seizures, and interictal discharges (IDs).

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Section: The Impact Of Seizuresmentioning

confidence: 74%

Mechanisms Responsible for Cognitive Impairment in Epilepsy

Lenck-Santini

Scott

2015

Cold Spring Harb Perspect Med

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“…However, mossy fiber sprouting occurs in adult animals 39,40,43. Extratemporal areas can also be affected, including increased prefrontal cortex thickness, synaptic plasticity alterations, and decreased behavioral flexibility 45,46. These data indicate substantial changes in prefrontal cortex function, which may be an important substrate of cognitive deficits in humans with a history of infant or juvenile seizures 45.…”

Section: Chemoconvulsantsmentioning

confidence: 99%

Animal models of epilepsy: use and limitations

Kandratavicius¹,

Balista²,

Lopes-Aguiar³

et al. 2014

NDT

379

241

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Epilepsy is a chronic neurological condition characterized by recurrent seizures that affects millions of people worldwide. Comprehension of the complex mechanisms underlying epileptogenesis and seizure generation in temporal lobe epilepsy and other forms of epilepsy cannot be fully acquired in clinical studies with humans. As a result, the use of appropriate animal models is essential. Some of these models replicate the natural history of symptomatic focal epilepsy with an initial epileptogenic insult, which is followed by an apparent latent period and by a subsequent period of chronic spontaneous seizures. Seizures are a combination of electrical and behavioral events that are able to induce chemical, molecular, and anatomic alterations. In this review, we summarize the most frequently used models of chronic epilepsy and models of acute seizures induced by chemoconvulsants, traumatic brain injury, and electrical or sound stimuli. Genetic models of absence seizures and models of seizures and status epilepticus in the immature brain were also examined. Major uses and limitations were highlighted, and neuropathological, behavioral, and neurophysiological similarities and differences between the model and the human equivalent were considered. The quest for seizure mechanisms can provide insights into overall brain functions and consciousness, and animal models of epilepsy will continue to promote the progress of both epilepsy and neurophysiology research.

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“…Previous work with this model showed that rats with ELS have persistent increased excitation (Isaeva et al 2010) and decreased GABA currents (Isaeva et al 2009) in the neocortex and a substantially reduced lower seizure threshold (Holmes et al 2015). ELS also have been shown to increase short-term plasticity in the mesial prefrontal cortex (mPFC) (Hernan et al 2013). Alterations in short-term plasticity in the mPFC have been associated with changes in hippocampal-PFC synchrony (Sigurdsson et al 2010;Fenelon et al 2013).…”

Section: Altered E/i Balance and Connectivitymentioning

confidence: 99%

Epilepsy and Autism

Buckley

Holmes

2016

Cold Spring Harb Perspect Med

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Epilepsy and autistic spectrum disorder frequently coexist in the same individual. Electroencephalogram (EEG) epileptiform activity is also present at a substantially higher rate in children with autism than normally developing children. As with epilepsy, there are a multitude of genetic and environmental factors that can result in autistic spectrum disorder. There is growing consensus from both animal and clinical studies that autism is a disorder of aberrant connectivity. As measured with functional magnetic resonance imaging (MRI) and EEG, the brain in autistic spectrum disorder may be under-or overconnected or have a mixture of over-and underconnectivity. In the case of comorbid epilepsy and autism, an imbalance of the excitatory/inhibitory (E/I) ratio in selected regions of the brain may drive overconnectivity. Understanding the mechanism by which altered connectivity in individuals with comorbid epilepsy and autistic spectrum disorder results in the behaviors specific to the autistic spectrum disorder remains a challenge.

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Altered short-term plasticity in the prefrontal cortex after early life seizures

Cited by 39 publications

References 69 publications

Mechanisms Responsible for Cognitive Impairment in Epilepsy

Mechanisms Responsible for Cognitive Impairment in Epilepsy

Animal models of epilepsy: use and limitations

Epilepsy and Autism

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