Pacemaker GABA synaptic activity may contribute to network synchronization in pediatric cortical dysplasia

NEUROBIOLOGY OF DISEASE

卷:62

Article

Cepeda, Carlos¹  Chen, Jane Y.¹  Wu, Joyce Y.²  Fisher, Robin S.¹  Vinters, Harry V.³  Mathern, Gary W.^1,4,5  Levine, Michael S.^1,5 

[1] Univ Calif Los Angeles, David Geffen Sch Med, Brain Res Inst, Intellectual & Dev Disabil Res Ctr, Los Angeles, CA 90095 USA

[2] Univ Calif Los Angeles, David Geffen Sch Med, Mattel Childrens Hosp, Div Pediat Neurol, Los Angeles, CA 90095 USA

[3] Univ Calif Los Angeles, David Geffen Sch Med, Sect Neuropathol, Dept Neurol, Los Angeles, CA 90095 USA

[4] Univ Calif Los Angeles, David Geffen Sch Med, Mattel Childrens Hosp, Dept Neurosurg, Los Angeles, CA 90095 USA

[5] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Behav Sci, Los Angeles, CA 90095 USA

关键词: Pediatric epilepsy;    Cortical dysplasia;    Synaptic activity;    GABA;    Synchrony;    Development;   

DOI  :  10.1016/j.nbd.2013.10.001

来源: Elsevier

【 摘 要 】

Spontaneous pacemakery-aminobutyric acid (GABA) receptor-mediated synaptic activity (PGA) occurs in a subset of tissue samples from pediatric epilepsy surgery patients. In the present study, based on single-cell electrophysiological recordings from 120 cases, we describe the etiologies, cell types, and primary electrophysiological features of PGA. Cells displaying PGA occurred more frequently in the areas &greatest anatomical abnormality in cases of focal cortical dysplasia (CD), often associated with hemimegalencephaly (HME), and only rarely in nonCD etiologies. PGA was characterized by rhythmic synaptic events (5-10 Hz) and was observed in normal-like, dysmorphic cytomegalic, and immature pyramidal neurons. PGA was action potential-dependent, mediated by GABAA receptors, and unaffected by antagonism of glutamate receptors. We propose that PGA is a unique electrophysiological characteristic associated with CD and HME. It could represent an abnormal signal that may contribute to epileptogenesis in malformed postnatal cortex by facilitating pyramidal neuron synchrony. (C) 2013 Elsevier Inc. All rights reserved.

【 授权许可】

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