Interictal-like network activity and receptor expression in the epileptic human lateral amygdala.

作者: S. Graebenitz , O. Kedo , E.-J. Speckmann , A. Gorji , H. Panneck

DOI: 10.1093/BRAIN/AWR202

关键词: Glutamate receptorKainate receptorMetabotropic receptorReceptor expressionReceptor antagonistReceptorHippocampusChemistryBicucullineNeuroscience

摘要: While the amygdala is considered to play a critical role in temporal lobe epilepsy, conclusions on underlying pathophysiological mechanisms have been derived largely from experimental animal studies. Therefore, present study aimed characterize synaptic network interactions, focusing spontaneous interictal-like activity, and expression profile of transmitter receptors human lateral relation epilepsy. Electrophysiological recordings, obtained intra-operatively vivo patients with medically intractable revealed existence interictal activity hippocampus. For vitro analyses, slices were prepared surgically resected specimens, sections individual specimens used for electrophysiological receptor autoradiographic analyses histological visualization major amygdaloid nuclei verification recording sites. In amygdala, appeared as slow rhythmic field potentials at an average frequency 0.39 Hz, which occurred different sites various degrees synchronization 33.3% tested slices. Pharmacological blockade glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, but not N-methyl-D-aspartate abolished while γ-aminobutyric A-type antagonist bicuculline resulted dampening followed by highly synchronous patterns during washout. Receptor analysis significantly higher acid, kainate, metabotropic type 2/3, muscarinic 2 adrenoceptor α(1) densities, whereas muscarinergic 3 serotonergic 1A densities lower epileptic comparison autopsy controls. Concerning agonist binding was unaltered downregulated suggesting altered high/low-affinity state ratio concomitant reduced pool total receptors. Together these data indicate abnormal pattern function nucleus patients, involving alterations may give rise domains discharges contributing seizure amygdala.

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