Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

Tian, Yong; Guo, Songxue; Li, Jianru; Du, Hang-Gen; Wang, Chaohui; Zhang, Jianmin; Wu, Qun

doi:10.1016/j.brainres.2015.06.007

Cited by 27 publications

(23 citation statements)

References 53 publications

(83 reference statements)

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“…KCC2 expression is susceptible to CNS injury (Galeffi et al, 2004 ; Bonislawski et al, 2007 ; Papp et al, 2008 ; Boulenguez et al, 2010 ; Jaenisch et al, 2010 ; Ma et al, 2014 ; Tian et al, 2015 ), and reduced KCC2 has been reported in CA3 pyramidal neurons resected from humans with epilepsy (Huberfeld et al, 2007 ), and in peri-tumoral cortex (Pallud et al, 2014 ; Campbell et al, 2015 ). To determine if prenatal TSHI altered CA3 KCC2 expression on CA3 neurons in our model, we performed double-labeling immunohistochemistry.…”

Section: Resultsmentioning

confidence: 99%

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Prenatal Hypoxia–Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone

Jantzie

Getsy

Denson

et al. 2015

Front. Cell. Neurosci.

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Infants who suffer perinatal brain injury, including those with encephalopathy of prematurity, are prone to chronic neurological deficits, including epilepsy, cognitive impairment, and behavioral problems, such as anxiety, inattention, and poor social interaction. These deficits, especially in combination, pose the greatest hindrance to these children becoming independent adults. Cerebral function depends on adequate development of essential inhibitory neural circuits and the appropriate amount of excitation and inhibition at specific stages of maturation. Early neuronal synaptic responses to γ-amino butyric acid (GABA) are initially excitatory. During the early postnatal period, GABAAR responses switch to inhibitory with the upregulation of potassium-chloride co-transporter KCC2. With extrusion of chloride by KCC2, the Cl− reversal potential shifts and GABA and glycine responses become inhibitory. We hypothesized that prenatal hypoxic–ischemic brain injury chronically impairs the developmental upregulation of KCC2 that is essential for cerebral circuit formation. Following late gestation hypoxia–ischemia (HI), diffusion tensor imaging in juvenile rats shows poor microstructural integrity in the hippocampal CA3 subfield, with reduced fractional anisotropy and elevated radial diffusivity. The loss of microstructure correlates with early reduced KCC2 expression on NeuN-positive pyramidal neurons, and decreased monomeric and oligomeric KCC2 protein expression in the CA3 subfield. Together with decreased inhibitory post-synaptic currents during a critical window of development, we document for the first time that prenatal transient systemic HI in rats impairs hippocampal CA3 inhibitory tone. Failure of timely development of inhibitory tone likely contributes to a lower seizure threshold and impaired cognitive function in children who suffer perinatal brain injury.

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Section: Resultsmentioning

confidence: 99%

“…Notably, increases in spontaneous IPSC frequency often reflect increased inhibitory tone (Alvarez-Dolado et al, 2006 ). KCC2 and GABA A R maturation are linked in models of CNS injury and repair (Papp et al, 2008 ; Jantzie et al, 2015 ; Tian et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Prenatal Hypoxia–Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone

Jantzie

Getsy

Denson

et al. 2015

Front. Cell. Neurosci.

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“…Furthermore, we also identified the potential drugs for inhibiting PPARG, consisting of the most negatively correlated adiphenine, DL-PPMP, decitabine and topiramate. Several studies have demonstrated topiramate could attenuate oxidative damage, inflammation and neuronal cell death (Motaghinejad M 2016;Tian et al 2015), indicating topiramate may also be an underlying drug for PPARG-related AHL.…”

Section: And Mir-29bmentioning

confidence: 99%

Peer Review #1 of "Cmah deficiency may lead to age-related hearing loss by influencing miRNA-PPAR mediated signaling pathway (v0.2)"

Mishra¹

2019

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Background: Previous evidence has indicated CMP-Neu5Ac hydroxylase (Cmah) disruption inducesaging-related hearing loss (AHL). However, its function mechanisms remain unclear. This study was to explore the mechanisms of AHL by using microarray analysis in the Cmah deficiency animal model. Methods: Microarray dataset GSE70659 was available from the Gene Expression Omnibus database, including cochlear tissues from wild-type and Cmah-null C57BL/6J mice with old age (12 months, n = 3). Differentially expressed genes (DEGs) were identified using the Linear Models for Microarray data method and protein-protein interaction (PPI) network was constructed using data from the Search Tool for the Retrieval of Interacting Genes database followed by module analysis. Kyoto encyclopedia of genes and genomes pathway enrichment analysis was performed using The Database for Annotation, Visualization and Integrated Discovery. The upstream miRNAs and potential small-molecule drugs were predicted by miRwalk2.0 and Connectivity Map, respectively. Results: A total of 799 DEGs (449 upregulated and 350 downregulated) were identified. Upregulated DEGs were involved in Cell adhesion molecules (ICAM1, intercellular adhesion molecule 1) and tumor necrosis factor (TNF) signaling pathway (FOS, FBJ osteosarcoma oncogene; ICAM1), while downregulated DEGs participated in PPAR signaling pathway (PPARG, peroxisome proliferator-activated receptor gamma). A PPI network was constructed, in which FOS, ICAM1 and PPARG were ranked as hub genes and PPARG was a transcription factor to regulate other target genes (ICAM1, FOS). Function analysis of two significant modules further demonstrated PPAR signaling pathway was especially important. Furthermore, mmu-miR-130b-3p, mmu-miR-27a-3p, mmu-miR-27b-3p and mmu-miR-721 were predicted to regulate PPARG. Topiramate were speculated to be a potential small-molecule drug to reverse DEGs in AHL. Conclusions: PPAR mediated signaling pathway may be an important mechanism for AHL. Downregulation of the above miRNAs and use of topiramate may be potential treatment

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“…Western blot analysis by Yong Tien, et al (2015) revealed multiple neuroinflammatory components following subarachnoid hemorrhage. The NKCC1 and KCC2 ratio shifts were significant, demonstrating changes of their protein expression [53]. Western blot analysis characterized a decline in KCC2 expression and increase expression in NKCC1 following induced subarachnoid hemorrhage in their rat model.…”

Section: Nkcc1 and Kcc2 Co-transporter Ion Channelsmentioning

confidence: 99%

Temporal Lobe Epilepsy, Stroke, and Traumatic Brain Injury: Mechanisms of Hyperpolarized, Depolarized, and Flow-Through Ion Channels Utilized as Tri-Coordinate Biomarkers of Electrophysiologic Dysfunction

Sizemore

Lucke‐Wold²,

Rosen³

et al. 2018

obm neurobiol

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The brain is an integrated network of multiple variables that when compromised create a diseased state. The neuropathology of temporal lobe epilepsy (TLE), stroke, and traumatic brain injury (TBI) demonstrate both similarity and complexity that reflects this integrated variability; TLE with its live human tissue resection provides opportunity for translational science to demonstrate scale equivalent experimentation between the macroscopic world of clinical disease and the microscopic world of basic science. The extended value of this research is that the neuroinflammatory abnormalities that occur throughout astrocytes with hippocampal sclerosis and damaged or even reversed signaling pathways (inhibition to excitation such as with gaba-aminobutyric acid) are similar to those seen in post-stroke and TBI models. In evaluation of the epilepsy population this interconnectedness of pathology warrants further evaluation with collaborative efforts. This review summarizes patterns that could shift experimentation closer to the macro level of humanity, but still represent the micro world of genetics, epigenetics, and neuro-injury across etiologies of physiologic dysfunction such as TLE, stroke, and TBI with evaluation of cell function using electrophysiology. In conclusion we demonstrate the plausibility of electrophysiologic voltage and current measurement of brain tissue by patch clamp analysis to specify actual electrophysiologic function for comparison to electroencephalography in order to aid neurologic evaluation. Finally, we discuss the opportunity with multiscale modeling to display integration of the hyperpolarization cyclic-nucleotide gated channel, the depolarized calcium channels, and sodium-potassium-chloride-one/potassium-chloride-two co-transporter channels as potential mechanisms utilized as tri-coordinate biomarkers with these three forms of neurologic disease at a molecular scale of electrophysiologic pathology.

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Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

Cited by 27 publications

References 53 publications

Prenatal Hypoxia–Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone

Prenatal Hypoxia–Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone

Peer Review #1 of "Cmah deficiency may lead to age-related hearing loss by influencing miRNA-PPAR mediated signaling pathway (v0.2)"

Temporal Lobe Epilepsy, Stroke, and Traumatic Brain Injury: Mechanisms of Hyperpolarized, Depolarized, and Flow-Through Ion Channels Utilized as Tri-Coordinate Biomarkers of Electrophysiologic Dysfunction

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