Distinct regulation of metabotropic glutamate receptor (mGluR1 alpha) in the developing limbic system following multiple early-life seizures

Avallone, Jennifer; Gashi, Eleonora; Magrys, Bonaventure; Friedman, Linda K.

doi:10.1016/j.expneurol.2006.05.033

Cited by 21 publications

(5 citation statements)

References 61 publications

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“…Results from a study in rodents, however, showed that mGluR1 expression might peak in the first postnatal week, whereas mGluR2, mGluR3 and mGluR5 levels mature by the second postnatal week 43. Agonists of group I mGluRs exert proconvulsant effects, suggesting that elevated levels of receptors from this group might have a role in early excitability.…”

Section: Seizure Susceptibility Factorsmentioning

confidence: 99%

Epileptogenesis in the immature brain: emerging mechanisms

2009

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Epileptogenesis is defined as the process of developing epilepsy-a disorder characterized by recurrent seizures-following an initial insult. Seizure incidence during the human lifespan is at its highest in infancy and childhood. Animal models of epilepsy and human tissue studies suggest that epileptogenesis involves a cascade of molecular, cellular and neuronal network alterations. Within minutes to days following the initial insult, there are acute early changes in neuronal networks, which include rapid alterations to ion channel kinetics as a result of membrane depolarization, posttranslational modifications to existing functional proteins, and activation of immediate early genes. Subacute changes occur over hours to weeks, and include transcriptional events, neuronal death and activation of inflammatory cascades. The chronic changes that follow over weeks to months include anatomical changes, such as neurogenesis, mossy fiber sprouting, network reorganization, and gliosis. These epileptogenic processes are developmentally regulated and might contribute to differences in epileptogenesis between adult and developing brains. Here we review the factors responsible for enhanced seizure susceptibility in the developing brain, and consider age-specific mechanisms of epileptogenesis. An understanding of these factors could yield potential therapeutic targets for the prevention of epileptogenesis and also provide biomarkers for identifying patients at risk of developing epilepsy or for monitoring disease progression.

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Section: Seizure Susceptibility Factorsmentioning

confidence: 99%

Epileptogenesis in the immature brain: emerging mechanisms

2009

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Section: Preclinical Insights Into the E:i Ratio In Developmentmentioning

confidence: 99%

“…The abundance of presynaptic mGluR1α receptors in developing rat brains up to the ninth day after birth (human age: term infant), particularly on hippocampal interneurons [115], may facilitate presynaptic release of GABA, and may explain the resistance of the developing brain to seizure-induced damage in spite of increased susceptibility to seizures. mGluR2, mGluR3, and mGluR5 mature by 15 days after birth in rodents (human age: 0–24 months) [115]. Recent evidence indicates that cathodal tDCS-induced LTD is primarily mediated by mGluR5 receptors [116] and, thus, direct current stimulation protocols may not be less, if at all, effective during the first 2 years after birth in humans.…”

Section: Preclinical Insights Into the E:i Ratio In Developmentmentioning

confidence: 99%

Transcranial Magnetic and Direct Current Stimulation in Children

Hameed

Dhamne

Gersner

et al. 2017

Curr Neurol Neurosci Rep

110

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Promising results in adult neurologic and psychiatric disorders are driving active research into transcranial brain stimulation techniques, particularly transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS), in childhood and adolescent syndromes. TMS has realistic utility as an experimental tool tested in a range of pediatric neuropathologies such as perinatal stroke, depression, Tourette syndrome, and autism spectrum disorder (ASD). tDCS has also been tested as a treatment for a number of pediatric neurologic conditions, including ASD, attention-deficit/hyperactivity disorder, epilepsy, and cerebral palsy. Here, we complement recent reviews with an update of published TMS and tDCS results in children, and discuss developmental neuroscience considerations that should inform pediatric transcranial stimulation.

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“…Nevertheless, targeting mGluR2/3 receptors for the treatment of comorbid depression may be problematic in TLE patients because these receptors inhibit glutamate release through presynaptic mechanisms (Campo et al, ) and may be upregulated in the epileptic LA to counteract increased excitability. Confirmation of changes in types of mGluRs may also be necessary because amygdala neurons showed reduced mGluRII‐induced hyperpolarization, whereas group I mGluR responses (mGluR1/5 glutamate receptors) and levels (mGluR1α) were increased in experimental epilepsy (Holmes et al, ; Avallone et al, ).…”

Section: Mechanisms Contributing To Comorbid Emotional Changes In Tlementioning

confidence: 99%

Contribution of amygdala pathology to comorbid emotional disturbances in temporal lobe epilepsy

Yilmazer-Hanke

O’Loughlin

McDermott

2015

J of Neuroscience Research

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The amygdala contributes to the generation and propagation of epileptiform activity in temporal lobe epilepsy (TLE). Ictal symptoms such as fear, dreamy states (déjà vu, memory flashbacks, experiential hallucinations), epigastric auras, or sympathetic outflow with cardiovascular changes are often linked to a seizure focus in the amygdala. However, the amygdala may also play a role in comorbid anxiety, depression, and other psychiatric symptoms experienced in the interictal phase, especially in pharmacoresistant TLE. The few studies available on TLE-related alterations in surgical amygdala specimens indicate loss of both excitatory spiny projection neurons as well as interneurons in nuclei with a cortex-like architecture, which may influence mechanisms of feedforward and feedback inhibition. Studies of the human amygdala indicate global alterations in the density of AMPA/kainate, metabotropic glutamate, γ-aminobutyric acid type A (GABAA ), muscarinic M2 and M3, serotonergic 5-HT1A, and adrenergic α1 receptors. Also, amygdala GABAergic and neuropeptide Y (NPY) systems affected in human TLE are both involved in antiepileptic and anxiolytic effects. Experimental and human positron emission tomography studies indicate changes in amygdala serotonergic, NPY Y1 receptor, neurokinin, and opioid systems in emotional disturbances in TLE. Of particular interest is the reduction in amygdala volume in conjunction with ictal fear, seizure focus in the amygdala, and amygdala and hippocampal sclerosis in TLE patients. In contrast, patients with interictal depression often have an intact or even enlarged amygdala and a negative MRI associated with amygdala hypometabolism, which can be associated with limbic autoimmune encephalitis. These findings suggest a differential role of TLE-related amygdala changes in ictal and interictal emotional disturbances.

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Distinct regulation of metabotropic glutamate receptor (mGluR1 alpha) in the developing limbic system following multiple early-life seizures

Cited by 21 publications

References 61 publications

Epileptogenesis in the immature brain: emerging mechanisms

Epileptogenesis in the immature brain: emerging mechanisms

Transcranial Magnetic and Direct Current Stimulation in Children

Contribution of amygdala pathology to comorbid emotional disturbances in temporal lobe epilepsy

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