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NMDA receptor‐mediated transmission contributes to network ‘hyperexcitability’ in the rat insular cortex
Author(s) -
Inaba Yuji,
De Guzman Philip,
Avoli Massimo
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.04607.x
Subject(s) - neuroscience , depolarization , nmda receptor , perirhinal cortex , neurotransmission , intracellular , local field potential , insular cortex , biology , chemistry , receptor , biophysics , microbiology and biotechnology , temporal lobe , biochemistry , epilepsy
The insular cortex (IC) plays distinct roles under physiological and pathological conditions. However, the mechanisms regulating excitability in this area remain unknown. By employing field potential and sharp‐electrode intracellular recordings in horizontal rat brain slices comprising the IC and the perirhinal cortex, we studied here the intrinsic and network characteristics of neurons in the agranular IC. These cells generated regular action potential firing with weak adaptation during intracellular injection of depolarizing current pulses, and were pyramidal in shape when neurobiotin filled. Spontaneous, field events (duration = 2.3 ± 0.25 s; intervals of occurrence = 44.9 ± 6.3 s) were identified in 22/52 slices and corresponded in IC neurons to intracellular depolarizations with action potential firing. Similar field and intracellular discharges were elicited in all slices by electrical stimuli. Antagonizing N ‐methyl‐ d ‐aspartate (NMDA) receptors blocked the spontaneous activity and reduced or abolished the stimulus‐induced discharges. In the latter cases, stimuli elicited depolarizing events that became hyperpolarizing at about −64 mV, suggesting the contribution of γ‐aminobutyric acid (GABA) A receptor‐mediated conductances. Our findings identify for the first time some functional properties of agranular IC neurons and point at a powerful NMDA receptor‐mediated mechanism implementing network hyperexcitability. This feature may contribute to the role of IC in neurological disorders.