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Enhancement of Asynchronous Release from Fast-spiking Interneuron in Human and Rat Epileptic Neocortex

Overview
Journal PLoS Biol
Specialty Biology
Date 2012 May 17
PMID 22589699
Citations 35
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Abstract

Down-regulation of GABAergic inhibition may result in the generation of epileptiform activities. Besides spike-triggered synchronous GABA release, changes in asynchronous release (AR) following high-frequency discharges may further regulate epileptiform activities. In brain slices obtained from surgically removed human neocortical tissues of patients with intractable epilepsy and brain tumor, we found that AR occurred at GABAergic output synapses of fast-spiking (FS) neurons and its strength depended on the type of connections, with FS autapses showing the strongest AR. In addition, we found that AR depended on residual Ca²⁺ at presynaptic terminals but was independent of postsynaptic firing. Furthermore, AR at FS autapses was markedly elevated in human epileptic tissue as compared to non-epileptic tissue. In a rat model of epilepsy, we found similar elevation of AR at both FS autapses and synapses onto excitatory neurons. Further experiments and analysis showed that AR elevation in epileptic tissue may result from an increase in action potential amplitude in the FS neurons and elevation of residual Ca²⁺ concentration. Together, these results revealed that GABAergic AR occurred at both human and rat neocortex, and its elevation in epileptic tissue may contribute to the regulation of epileptiform activities.

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References
1.
Buhl E, Otis T, Mody I . Zinc-induced collapse of augmented inhibition by GABA in a temporal lobe epilepsy model. Science. 1996; 271(5247):369-73. DOI: 10.1126/science.271.5247.369. View

2.
Chen S, Su H, Yue C, Remy S, Royeck M, Sochivko D . An increase in persistent sodium current contributes to intrinsic neuronal bursting after status epilepticus. J Neurophysiol. 2010; 105(1):117-29. DOI: 10.1152/jn.00184.2010. View

3.
Geiger J, Jonas P . Dynamic control of presynaptic Ca(2+) inflow by fast-inactivating K(+) channels in hippocampal mossy fiber boutons. Neuron. 2001; 28(3):927-39. DOI: 10.1016/s0896-6273(00)00164-1. View

4.
Kapfer C, Glickfeld L, Atallah B, Scanziani M . Supralinear increase of recurrent inhibition during sparse activity in the somatosensory cortex. Nat Neurosci. 2007; 10(6):743-53. PMC: 3518866. DOI: 10.1038/nn1909. View

5.
Sun J, Pang Z, Qin D, Fahim A, Adachi R, Sudhof T . A dual-Ca2+-sensor model for neurotransmitter release in a central synapse. Nature. 2007; 450(7170):676-82. PMC: 3536472. DOI: 10.1038/nature06308. View