Astrocytes are abundant cells in the brain that regulate multiple aspects of neural tissue homeostasis by providing structural and metabolic support to neurons, maintaining synaptic environments and regulating blood flow. Recent evidence indicates that astrocytes also actively participate in brain functions and play a key role in brain disease by responding to neuronal activities and brain insults. Astrocytes become reactive in response to injury and inflammation, which is typically described as hypertrophy with increased expression of glial fibrillary acidic protein (GFAP). Reactive astrocytes are frequently found in many neurological disorders and are a hallmark of brain disease. Furthermore, reactive astrocytes may drive the initiation and progression of disease processes. Recent improvements in the methods to visualize the activity of reactive astrocytes in situ and in vivo have helped elucidate their functions. Ca2+ signals in reactive astrocytes are closely related to multiple aspects of disease and can be a good indicator of disease severity/state. In this review, we summarize recent findings concerning reactive astrocyte Ca2+ signals. We discuss the molecular mechanisms underlying aberrant Ca2+ signals in reactive astrocytes and the functional significance of aberrant Ca2+ signals in neurological disorders.
Extensive activation of glial cells during a latent period has been well documented in various animal models of epilepsy. However, it remains unclear whether activated glial cells contribute to epileptogenesis; i.e., the chronically persistent process leading to epilepsy. Particularly, it is not clear whether interglial communication between different types of glial cells contributes to epileptogenesis, as past literature mainly focused on one type of glial cell. Here, we show that temporally distinct activation profiles of microglia and astrocytes collaboratively contribute to epileptogenesis in a drug-induced status epilepticus model. We found that reactive microglia appeared first, followed by reactive astrocytes and increased susceptibility to seizures. Reactive astrocytes exhibited larger Ca 2+ signals mediated by IP3R2, whereas deletion of this type of Ca 2+ signaling reduced seizure susceptibility after status epilepticus.Immediate, but not late, pharmacological inhibition of microglial activation prevented subsequent reactive astrocytes, aberrant astrocyte Ca 2+ signaling, and the enhanced seizure susceptibility. These findings indicate that the sequential activation of glial cells constitutes a cause of epileptogenesis after status epilepticus. Thus, our findings suggest that the therapeutic target to 4 prevent epilepsy after status epilepticus should be shifted from microglia (early phase) to astrocytes (late phase).
Parental fears that the death of their child was imminent and the misperception of FS as a serious, life-threatening condition indicate a lack of knowledge regarding FS. Organizing parental support groups and effective educational intervention programs for parents should be given priority in the care of children with FS.
ABPE Atypical benign partial epilepsy CSWS Continuous spikes and waves during slow-wave sleep LKS Landau-Kleffner syndrome AIM Although the prognosis for rolandic epilepsy is regarded to be favourable, a small proportion of cases that initially present as rolandic epilepsy evolve into atypical benign partial epilepsy (ABPE) of childhood. The purpose of our study was to determine electroencephalogram (EEG) criteria in relation to atypical seizure manifestations, and cognitive and behavioural problems in rolandic epilepsy.
METHODSThe rolandic epilepsy group consisted of 10 children (mean age 5y 6mo, SD 1y 1mo, median age 5y 5mo; six males, four females). The ABPE group comprised five children (mean age 5y, SD 1y 2mo, median age 4y 5mo; three males, two females). We recorded the number of spikes, the locations of spikes, and the duration of the spike activity. The Wechsler Intelligence Scale for Children-Third Edition or the Wechsler Preschool and Primary Scale of Intelligence, depending on age, was administered to all children at the onset of seizures and every year thereafter. The diagnosis of attention-deficit-hyperactivity disorder was made according to the DSM-IV. RESULTS Significant correlations were found between atypical clinical features and extended periods of high-frequency paroxysmal EEG abnormalities (>24mo after onset; p<0.01) and frontal EEG focus (>10mo after onset; p<0.003).INTERPRETATION A combination of spike rate and extended periods of high-frequency paroxysmal EEG abnormalities may predict the evolution of atypical rolandic epilepsy.
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