Increased pCREB expression and the spontaneous epileptiform activity in a BCNU‐treated rat model of cortical dysplasia

Cortical dysplasias (CDs) represent a wide range of cortical abnormalities that closely correlate with intractable epilepsy. Rats prenatally exposed to 1‐3‐bis‐chloroethyl‐nitrosurea (BCNU) represent an injury‐based model that reproduces many histopathologic features of human CD. Previous studies reported in vivo hyperexcitability in this model, but in vivo epileptogenicity has not been confirmed.

[1]  A. Represa,et al.  Normotopic cortex is the major contributor to epilepsy in experimental double cortex , 2014, Annals of neurology.

[2]  Yangmei Chen,et al.  Expression of p-CREB and activity-dependent miR-132 in temporal lobe epilepsy. , 2014, International journal of clinical and experimental medicine.

[3]  R. Moroni,et al.  Genesis of Heterotopia in BCNU Model of Cortical Dysplasia, Detected by Means of in utero Electroporation , 2013, Developmental Neuroscience.

[4]  G. Battaglia,et al.  Intrinsic epileptogenicity of dysplastic cortex: Converging data from experimental models and human patients , 2013, Epilepsia.

[5]  Satoshi O. Suzuki,et al.  Spontaneous seizures in a rat model of multiple prenatal freeze lesioning , 2013, Epilepsy Research.

[6]  R. Moroni,et al.  Cytoarchitectural, behavioural and neurophysiological dysfunctions in the BCNU‐treated rat model of cortical dysplasia , 2013, The European journal of neuroscience.

[7]  J. Loeb,et al.  Layer-Specific CREB Target Gene Induction in Human Neocortical Epilepsy , 2012, Journal of Neuroscience.

[8]  Jing Hua,et al.  Electrical, molecular and behavioral effects of interictal spiking in the rat , 2012, Neurobiology of Disease.

[9]  P. Schwartzkroin,et al.  Are developmental dysplastic lesions epileptogenic? , 2012, Epilepsia.

[10]  R. Kuzniecky,et al.  A developmental and genetic classification for malformations of cortical development: update 2012 , 2012, Brain : a journal of neurology.

[11]  P. Schwartzkroin,et al.  Initiation of epileptiform activity in a rat model of periventricular nodular heterotopia , 2011, Epilepsia.

[12]  Annamaria Vezzani,et al.  Status epilepticus-induced pathologic plasticity in a rat model of focal cortical dysplasia. , 2011, Brain : a journal of neurology.

[13]  R. Moroni,et al.  In vivo detection of cortical abnormalities in BCNU-treated rats, model of cortical dysplasia, using manganese-enhanced magnetic resonance imaging , 2011, Neuroscience.

[14]  R. Moroni,et al.  Development of cortical malformations in BCNU-treated rat, model of cortical dysplasia , 2011, Neuroscience.

[15]  J. Roh,et al.  Role of cortical dysplasia in epileptogenesis following prolonged febrile seizure , 2010, Epilepsia.

[16]  S. Roper,et al.  Densities of glutamatergic and GABAergic presynaptic terminals are altered in experimental cortical dysplasia , 2010, Epilepsia.

[17]  M. Wong Animal models of focal cortical dysplasia and tuberous sclerosis complex: Recent progress toward clinical applications , 2009, Epilepsia.

[18]  Maria Thom,et al.  Malformations of cortical development and epilepsies: neuropathological findings with emphasis on focal cortical dysplasia. , 2009, Epileptic disorders : international epilepsy journal with videotape.

[19]  I. Najm,et al.  Single injection of a low dose of pentylenetetrazole leads to epileptogenesis in an animal model of cortical dysplasia , 2009, Epilepsia.

[20]  T. Yamamori,et al.  Expression of layer-specific markers in the adult neocortex of BCNU-Treated rat, a model of cortical dysplasia , 2009, Neuroscience.

[21]  John Bowyer,et al.  Introducing Black-Gold II, a highly soluble gold phosphate complex with several unique advantages for the histochemical localization of myelin , 2008, Brain Research.

[22]  H. Shigeto,et al.  Prenatal freeze lesioning produces epileptogenic focal cortical dysplasia , 2008, Epilepsia.

[23]  R. Moroni,et al.  Altered spatial distribution of PV‐cortical cells and dysmorphic neurons in the somatosensory cortex of BCNU‐treated rat model of cortical dysplasia , 2008, Epilepsia.

[24]  I. Najm,et al.  Pathophysiological Mechanisms of Focal Cortical Dysplasia: A Critical Review of Human Tissue Studies and Animal Models , 2007, Epilepsia.

[25]  H. Shigeto,et al.  Dissociation between in vitro and in vivo epileptogenicity in a rat model of cortical dysplasia. , 2007, Epileptic disorders : international epilepsy journal with videotape.

[26]  I. Najm,et al.  Altered Glutamate Receptor—Transporter Expression and Spontaneous Seizures in Rats Exposed to Methylazoxymethanol in Utero , 2007, Epilepsia.

[27]  Sorin Draghici,et al.  A common pattern of persistent gene activation in human neocortical epileptic foci , 2005, Annals of neurology.

[28]  H. Lüders,et al.  Severity of Histopathologic Abnormalities and In Vivo Epileptogenicity in the In Utero Radiation Model of Rats Is Dose Dependent , 2004, Epilepsia.

[29]  C. Liou,et al.  Long-term effects of early-life malnutrition and status epilepticus: assessment by spatial navigation and CREBSerine-133 phosphorylation , 2003 .

[30]  E. Benardete,et al.  Increased Excitability and Decreased Sensitivity to GABA in an Animal Model of Dysplastic Cortex , 2002, Epilepsia.

[31]  H. Lüders,et al.  Electroencephalographic Characterization of an Adult Rat Model of Radiation‐Induced Cortical Dysplasia , 2001, Epilepsia.

[32]  Y. Ben-Ari,et al.  Abnormal Connections in the Malformed Cortex of Rats with Prenatal Treatment with Methylazoxymethanol May Support Hyperexcitability , 1999, Developmental Neuroscience.

[33]  S. Roper In utero irradiation of rats as a model of human cerebrocortical dysgenesis: a review , 1998, Epilepsy Research.

[34]  H. Luhmann,et al.  Characterization of neuronal migration disorders in neocortical structures: I. Expression of epileptiform activity in an animal model , 1996, Epilepsy Research.

[35]  S. Moshé,et al.  Neuronal Migration Disorders Increase Susceptibility to Hyperthermia‐Induced Seizures in Developing Rats , 1996, Epilepsia.

[36]  M. Gutnick,et al.  Hyperexcitability in a model of cortical maldevelopment. , 1996, Cerebral cortex.

[37]  P. Schwartzkroin,et al.  Electrophysiology of CA1 pyramidal neurons in an animal model of neuronal migration disorders: prenatal methylazoxymethanol treatment , 1995, Epilepsy Research.

[38]  J. L. Stringer,et al.  Functional anatomy of hippocampal seizures , 1991, Progress in Neurobiology.

[39]  M. Witter The perforant path: projections from the entorhinal cortex to the dentate gyrus. , 2007, Progress in brain research.

[40]  C. Liou,et al.  Long-term effects of early-life malnutrition and status epilepticus: assessment by spatial navigation and CREB(Serine-133) phosphorylation. , 2003, Brain research. Developmental brain research.

[41]  G. Avanzini,et al.  Prenatal methylazoxymethanol treatment in rats produces brain abnormalities with morphological similarities to human developmental brain dysgeneses. , 1999, Journal of neuropathology and experimental neurology.