Dysfunctional epileptic neuronal circuits and dysmorphic dendritic spines are mitigated by platelet-activating factor receptor antagonism

Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void in understanding the cellular and molecular mechanisms that set in motion aberrant neuronal network formations during the course of limbic epileptogenesis (LE). Here we show in in vivo rodent models of LE that the phos...

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Published inScientific reports Vol. 6; no. 1; p. 30298
Main Authors Musto, Alberto E, Rosencrans, Robert F, Walker, Chelsey P, Bhattacharjee, Surjyadipta, Raulji, Chittalsinh M, Belayev, Ludmila, Fang, Zhide, Gordon, William C, Bazan, Nicolas G
Format Journal Article
LanguageEnglish
Published England Nature Publishing Group 22.07.2016
Subjects
Animals
Blood Platelets - metabolism
Dendritic Spines - metabolism
Dendritic Spines - pathology
Disease Models, Animal
Epilepsy, Temporal Lobe - drug therapy
Epilepsy, Temporal Lobe - genetics
Epilepsy, Temporal Lobe - metabolism
Epilepsy, Temporal Lobe - pathology
Hippocampus - drug effects
Hippocampus - metabolism
Hippocampus - pathology
Humans
Limbic Lobe - metabolism
Limbic Lobe - pathology
Medicin och hälsovetenskap
Mice
Neuronal Plasticity - drug effects
Neurons - drug effects
Neurons - metabolism
Neurons - pathology
Platelet Activating Factor - genetics
Platelet Activating Factor - metabolism
Platelet Membrane Glycoproteins - antagonists & inhibitors
Platelet Membrane Glycoproteins - genetics
Platelet Membrane Glycoproteins - metabolism
Receptors, G-Protein-Coupled - antagonists & inhibitors
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - metabolism
Online AccessGet full text

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Abstract Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void in understanding the cellular and molecular mechanisms that set in motion aberrant neuronal network formations during the course of limbic epileptogenesis (LE). Here we show in in vivo rodent models of LE that the phospholipid mediator platelet-activating factor (PAF) increases in LE and that PAF receptor (PAF-r) ablation mitigates its progression. Synthetic PAF-r antagonists, when administered intraperitoneally in LE, re-establish hippocampal dendritic spine density and prevent formation of dysmorphic dendritic spines. Concomitantly, hippocampal interictal spikes, aberrant oscillations, and neuronal hyper-excitability, evaluated 15-16 weeks after LE using multi-array silicon probe electrodes implanted in the dorsal hippocampus, are reduced in PAF-r antagonist-treated mice. We suggest that over-activation of PAF-r signaling induces aberrant neuronal plasticity in LE and leads to chronic dysfunctional neuronal circuitry that mediates epilepsy.
AbstractList Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void in understanding the cellular and molecular mechanisms that set in motion aberrant neuronal network formations during the course of limbic epileptogenesis (LE). Here we show in in vivo rodent models of LE that the phospholipid mediator platelet-activating factor (PAF) increases in LE and that PAF receptor (PAF-r) ablation mitigates its progression. Synthetic PAF-r antagonists, when administered intraperitoneally in LE, re-establish hippocampal dendritic spine density and prevent formation of dysmorphic dendritic spines. Concomitantly, hippocampal interictal spikes, aberrant oscillations, and neuronal hyper-excitability, evaluated 15–16 weeks after LE using multi-array silicon probe electrodes implanted in the dorsal hippocampus, are reduced in PAF-r antagonist-treated mice. We suggest that over-activation of PAF-r signaling induces aberrant neuronal plasticity in LE and leads to chronic dysfunctional neuronal circuitry that mediates epilepsy.
Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void in understanding the cellular and molecular mechanisms that set in motion aberrant neuronal network formations during the course of limbic epileptogenesis (LE). Here we show in in vivo rodent models of LE that the phospholipid mediator platelet-activating factor (PAF) increases in LE and that PAF receptor (PAF-r) ablation mitigates its progression. Synthetic PAF-r antagonists, when administered intraperitoneally in LE, re-establish hippocampal dendritic spine density and prevent formation of dysmorphic dendritic spines. Concomitantly, hippocampal interictal spikes, aberrant oscillations, and neuronal hyper-excitability, evaluated 15-16 weeks after LE using multi-array silicon probe electrodes implanted in the dorsal hippocampus, are reduced in PAF-r antagonist-treated mice. We suggest that over-activation of PAF-r signaling induces aberrant neuronal plasticity in LE and leads to chronic dysfunctional neuronal circuitry that mediates epilepsy.
Abstract Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void in understanding the cellular and molecular mechanisms that set in motion aberrant neuronal network formations during the course of limbic epileptogenesis (LE). Here we show in in vivo rodent models of LE that the phospholipid mediator platelet-activating factor (PAF) increases in LE and that PAF receptor (PAF-r) ablation mitigates its progression. Synthetic PAF-r antagonists, when administered intraperitoneally in LE, re-establish hippocampal dendritic spine density and prevent formation of dysmorphic dendritic spines. Concomitantly, hippocampal interictal spikes, aberrant oscillations, and neuronal hyper-excitability, evaluated 15–16 weeks after LE using multi-array silicon probe electrodes implanted in the dorsal hippocampus, are reduced in PAF-r antagonist-treated mice. We suggest that over-activation of PAF-r signaling induces aberrant neuronal plasticity in LE and leads to chronic dysfunctional neuronal circuitry that mediates epilepsy.
ArticleNumber 30298
Author Bhattacharjee, Surjyadipta
Rosencrans, Robert F
Walker, Chelsey P
Musto, Alberto E
Belayev, Ludmila
Fang, Zhide
Gordon, William C
Bazan, Nicolas G
Raulji, Chittalsinh M
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  organization: Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA
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  givenname: Chelsey P
  surname: Walker
  fullname: Walker, Chelsey P
  organization: Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA
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  givenname: Surjyadipta
  surname: Bhattacharjee
  fullname: Bhattacharjee, Surjyadipta
  organization: Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA
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  givenname: Chittalsinh M
  surname: Raulji
  fullname: Raulji, Chittalsinh M
  organization: Department of Pediatrics, Hematology-Oncology, Louisiana State University Health Sciences Center and Children's Hospital of New Orleans, New Orleans, Louisiana 70118, USA
– sequence: 6
  givenname: Ludmila
  surname: Belayev
  fullname: Belayev, Ludmila
  organization: Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA
– sequence: 7
  givenname: Zhide
  surname: Fang
  fullname: Fang, Zhide
  organization: Biostatistics, School of Public Health, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA
– sequence: 8
  givenname: William C
  surname: Gordon
  fullname: Gordon, William C
  organization: Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA
– sequence: 9
  givenname: Nicolas G
  surname: Bazan
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  organization: Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, 2020 Gravier Street, New Orleans, Louisiana 70112, USA
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Snippet Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void in understanding the cellular and molecular mechanisms that set in motion...
Abstract Temporal lobe epilepsy or limbic epilepsy lacks effective therapies due to a void in understanding the cellular and molecular mechanisms that set in...
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SubjectTerms Animals
Blood Platelets - metabolism
Dendritic Spines - metabolism
Dendritic Spines - pathology
Disease Models, Animal
Epilepsy, Temporal Lobe - drug therapy
Epilepsy, Temporal Lobe - genetics
Epilepsy, Temporal Lobe - metabolism
Epilepsy, Temporal Lobe - pathology
Hippocampus - drug effects
Hippocampus - metabolism
Hippocampus - pathology
Humans
Limbic Lobe - metabolism
Limbic Lobe - pathology
Medicin och hälsovetenskap
Mice
Neuronal Plasticity - drug effects
Neurons - drug effects
Neurons - metabolism
Neurons - pathology
Platelet Activating Factor - genetics
Platelet Activating Factor - metabolism
Platelet Membrane Glycoproteins - antagonists & inhibitors
Platelet Membrane Glycoproteins - genetics
Platelet Membrane Glycoproteins - metabolism
Receptors, G-Protein-Coupled - antagonists & inhibitors
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - metabolism
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Title Dysfunctional epileptic neuronal circuits and dysmorphic dendritic spines are mitigated by platelet-activating factor receptor antagonism
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