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Neural stem cells (NSCs) are one of the candidates for grafting in the realm of cell‐based therapy for temporal lobe epilepsy (TLE). Because NSCs can produce neurons synthesizing the inhibitory neurotransmitter γ‐aminobutyric acid (GABA) and cells secreting multiple neurotrophic factors, NSC grafting therapy has promise for restraining seizures and easing cognitive dysfunction in TLE. For an expanded...
Purpose: Past work has demonstrated that kainic acid (KA)–induced seizures could cause the enhancement of excitation and lead to neuronal death in rat hippocampus. To counteract such an imbalance between excitation and inhibition, we designed experiments by activating the inhibitory γ‐aminobutyric acid (GABA) receptor to investigate whether such activation suppresses the excitatory glutamate signaling...
Purpose: The objective of this study was to determine if levetiracetam (LEV) modulates brain γ‐aminobutyric acid (GABA) in patients with epilepsy.
Methods: Occipital GABA was assessed by protein magnetic resonance spectroscopy (1H‐MRS) in 16 patients with focal epilepsy at baseline and following the initiation of oral administration of LEV as monotherapy. Responder profiles were calculated as percentage...
Dravet syndrome is caused mainly by mutations of voltage‐gated Na+ channels (most of them targeting NaV1.1) and in few cases by mutations of γ‐aminobutyric acid (GABA)A receptor γ2 subunit. In vitro functional analysis has provided important information about the pathogenic mechanism of these mutations, which is in most cases consistent with reduced GABAergic inhibition and consequent hyperexcitability...
Purpose: The midline thalamus is an important component of the circuitry in limbic seizures, but it is unclear how synaptic modulation of the thalamus affects that circuitry. In this study, we wished to understand how synaptic modulation of the thalamus can affect interregional signaling and seizure spread in the limbic network.
Methods: We examined the effect of γ‐aminobutyric acid (GABA) modulation...
Purpose: γ‐Aminobutyric acid (GABA)ergic transmission plays an important role in the initiation of epileptic activity and the generation of ictal discharges. The functional alterations in the epileptiform hippocampus critically depend on GABAergic mechanisms and cation‐chloride cotransporters.
Methods: To understand the cellular basis of specific functional alterations in the epileptic hippocampus,...
Purpose: In temporal lobe epilepsy many somatostatin interneurons in the dentate gyrus die. However, some survive and sprout axon collaterals that form new synapses with granule cells. The functional consequences of γ‐aminobutyric acid (GABA)ergic synaptic reorganization are unclear. Development of new methods to suppress epilepsy‐related interneuron axon sprouting might be useful experimentally...
Purpose: The piriform cortex (PC) is known to be epileptic‐prone and it may be involved in the manifestation of limbic seizures. Herein, we have characterized some electrophysiologic and pharmacologic properties of the spontaneous epileptiform activity generated by PC networks maintained in vitro.
Methods: We performed field potential recordings from the PC in coronal or sagittal rat brain slices...
Gliomas are the most frequent primary brain tumors and most glioma patients have seizures. The origin and mechanisms of human glioma–related epilepsy are multifactorial and an intermix of oncologic and neuronal processes. In this brief review, we show that the infiltrated peritumoral neocortex appears to be the key structure for glioma‐related epileptic activity, which depends on the interactions...
Alterations in the balance of K‐Na‐2Cl cotransporter (NKCC1) and Na‐Cl cotransporter (KCC2) activity may cause depolarizing effect of γ‐aminobutyric Acid (GABA), and contribute to epileptogenesis in human temporal lobe epilepsy. NKCC1 facilitates accumulation of chloride inside neurons and favors depolarizing responses to GABA. In the current pilot study we provide the first documented look at efficacy...
Purpose: The K+ channel blocker 4‐aminopyridine (4AP) induces epileptiform synchronization in brain slices maintained in vitro without interfering with γ‐aminobutyric acid (GABA)A receptor–mediated inhibition and, actually, even enhancing it. The hypothesis that similar electrographic epileptiform patterns occur in vivo following systemic 4AP injection was tested here.
Methods: Sprague‐Dawley rats...
ObjectiveJuvenile myoclonic epilepsy (JME) has been considered to be a frontal variant of thalamocortical network dysfunction in epilepsy. Changes of γ‐aminobutyric acid (GABA)ergic neurotransmission may play a key role in this dysfunction. Magnetic resonance spectroscopy (MRS) is the only noninvasive method to measure GABA concentrations in different brain regions. We measured GABA and other metabolite...
ObjectiveGlutamate and γ‐aminobutyric acid (GABA) are the key neurotransmitter systems in the cortical‐thalamocortical network, involved in normal and pathologic oscillations such as spike‐wave discharges (SWDs), which characterize different forms of absence epilepsy. Metabotropic glutamate (mGlu) and GABA receptors are widely expressed within this network. Herein, we examined the effects of two selective...
ObjectiveThirty percent of patients with epilepsy are refractory to medication. The majority of these patients have mesial temporal lobe epilepsy (MTLE). This prompts for new pharmacologic targets, like ATP‐mediated signaling pathways, since the extracellular levels of the nucleotide dramatically increase during in vitro epileptic seizures. In this study, we investigated whether sodium‐dependent high‐affinity...
Objective
We investigated the role of chloride homeostasis in seizure progression and development of pharmacoresistant status epilepticus (SE) by pharmacologically targeting the Na‐K‐Cl cotransporter (NKCC1) with bumetanide. We also investigated the ability of bumetanide to restore the efficacy of diazepam following SE.
Methods
Kainic acid (KA)–induced SE in vivo and 0‐Mg2+‐induced seizure‐like...
Abnormally enhanced glutamatergic excitation is commonly believed to mark the onset of a focal seizure. This notion, however, is not supported by firm evidence, and it will be challenged here. A general reduction of unit firing has been indeed observed in association with low‐voltage fast activity at the onset of seizures recorded during presurgical intracranial monitoring in patients with focal,...
ObjectiveThe loop diuretic bumetanide has been reported to potentiate the antiseizure activity of phenobarbital in rodent models of neonatal seizures, most likely as a result of inhibition of the chloride importer Na‐K‐Cl cotransporter isoform 1 (NKCC1) in the brain. In view of the intractability of neonatal seizures, the preclinical findings prompted a clinical trial in neonates on bumetanide as...
Objective
Mutations of the KCNQ2 gene, which encodes the Kv7.2 subunit of voltage‐gated M‐type potassium channels, have been associated with epilepsy in the neonatal period. This developmental stage is unique in that the neurotransmitter gamma aminobutyric acid (GABA), which is inhibitory in adults, triggers excitatory action due to a reversed chloride gradient.
Methods
To examine whether KCNQ2...
Expediting pediatric access to new antiseizure drugs is particularly compelling, because epileptic seizures are the most common serious neurological symptom in children. Analysis of antiepileptic drug (AED) efficacy outcomes of randomized controlled trials, conducted during the past 20 years in different populations and a broad range of study sites and countries, has shown considerable consistency...
Objectives
Glutaric acidemia type I (GA‐I) is an inherited neurometabolic disorder caused by deficiency of glutaryl‐CoA dehydrogenase (GCDH) and characterized by increased levels of glutaric, 3‐OH‐glutaric, and glutaconic acids in the brain parenchyma. The increment of these organic acids inhibits glutamate decarboxylase (GAD) and consequently lowers the γ‐aminobutyric acid (GABA) synthesis. Untreated...
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