Morphometric changes and molecular mechanisms in rat models of idiopathic generalized epilepsy with absence seizures.

No abstract is available for this paper.

• Publication year

  2011

• Venue

  Neuroscience Letters

• Publication date

  2011-06-27

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/j.neulet.2011.02.039PMID 21354269
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• Thalamo-cortical network pathology in idiopathic generalized epilepsy: Insights from MRI-based morphometric correlation analysis

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• Amygdala volumes in childhood absence epilepsy.

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• Morphometric abnormalities and hyperanxiety in genetically epileptic rats: A model of psychiatric comorbidity?

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• Positive allosteric modulation of metabotropic glutamate 4 (mGlu4) receptors enhances spontaneous and evoked absence seizures.

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• Neuroactive steroids and GABAA receptor plasticity in the brain of the WAG/Rij rat, a model of absence epilepsy

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• Elevated anxiety and depressive-like behavior in a rat model of genetic generalized epilepsy suggesting common causation.

  2008cited by this paper
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• Correlation of T-channel coding gene expression, IT, and the low threshold Ca2+ spike in the thalamus of a rat model of absence epilepsy.

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• Early treatment suppresses the development of spike‐wave epilepsy in a rat model

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• A TASK3 channel (KCNK9) mutation in a genetic model of absence epilepsy

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• Generalized epilepsy with febrile seizures plus-associated sodium channel beta1 subunit mutations severely reduce beta subunit-mediated modulation of sodium channel function.

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• Glutamatergic alterations in the cortex of genetic absence epilepsy rats

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• Extended spectrum of idiopathic generalized epilepsies associated with CACNA1H functional variants

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• Inherited cortical HCN1 channel loss amplifies dendritic calcium electrogenesis and burst firing in a rat absence epilepsy model

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• Functional stabilization of weakened thalamic pacemaker channel regulation in rat absence epilepsy

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• The Mechanism of Carbamazepine Aggravation of Absence Seizures

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• SCN1A mutations and epilepsy

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• Genes and mutations in human idiopathic epilepsy.

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• Gating Effects of Mutations in the Cav3.2 T-type Calcium Channel Associated with Childhood Absence Epilepsy*

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• Chromosomal Mapping of Genetic Loci Controlling Absence Epilepsy Phenotypes in the WAG/Rij Rat

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• Polygenic Control of Idiopathic Generalized Epilepsy Phenotypes in the Genetic Absence Rats from Strasbourg (GAERS)

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• An impaired neocortical Ih is associated with enhanced excitability and absence epilepsy

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  2003cited by this paper
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• Genetic Animal Models for Absence Epilepsy: A Review of the WAG/Rij Strain of Rats

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• The genetics of human epilepsy.

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• Magnetic resonance spectroscopy and imaging of the thalamus in idiopathic generalized epilepsy.

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• Decreased expression of glutamate transporters in genetic absence epilepsy rats before seizure occurrence

  2002cited by this paper
• Cortical Focus Drives Widespread Corticothalamic Networks during Spontaneous Absence Seizures in Rats

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• Neuroprotective activity of metabotropic glutamate receptor ligands.

  2002cited by this paper
• Lack of the burst firing of thalamocortical relay neurons and resistance to absence seizures in mice lacking α1G T-type Ca2+ channels

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• Molecular mechanism of cAMP modulation of HCN pacemaker channels

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• Up-regulation of D3 dopaminergic receptor mRNA in the core of the nucleus accumbens accompanies the development of seizures in a genetic model of absence-epilepsy in the rat.

  2001cited by this paper
• Differential and age-dependent expression of hyperpolarization-activated, cyclic nucleotide-gated cation channel isoforms 1-4 suggests evolving roles in the developing rat hippocampus.

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• GABA(B)-receptor isoforms molecular architecture and distribution.

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• Induction of neonatal sodium channel II and III α‐isoform mRNAs in neurons and microglia after status epilepticus in the rat hippocampus

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• Lack of the burst firing of thalamocortical relay neurons and resistance to absence seizures in mice lacking alpha(1G) T-type Ca(2+) channels.

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• Dopamine in the striatum modulates seizures in a genetic model of absence epilepsy in the rat.

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• A Model of Chronic Spontaneous Petit Mal‐like Seizures in the Rat: Comparison with Pentylenetetrazol‐Induced Seizures

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