TY - JOUR
T1 - Quantitative dynamics and spatial profile of perisomatic GABAergic input during epileptiform synchronization in the CA1 hippocampus
AU - Marchionni, Ivan
AU - Maccaferri, Gianmaria
PY - 2009/12
Y1 - 2009/12
N2 - Perisomatic GABAergic input appears spared or even increased in intractable temporal lobe epilepsy, and has been suggested to contribute to the generation of pathological discharges. Nevertheless, its degree of functional activity during epileptiform synchronization has not been thoroughly investigated. Thus, it remains unclear how structural preservation or loss of domain-specific GABAergic input may affect the network. Here, we have taken advantage of a model of epileptiform activity . in vitro to quantify the charge transfer provided by perisomatic GABAA receptor-mediated input to CA1 pyramidal neurons during interictal-like bursts. By recording both firing in GABAergic interneurons and the charge transfer generated by unitary postsynaptic currents to target pyramidal cells, we have estimated the charge transfer that would be dynamically generated by the recruitment of the entire pool of perisomatic-targeting interneurons and the number of perisomatic-targeting interneurons that would be required to generate the experimentally observed GABAergic input. In addition, we have recorded and compared the dynamics and charge density of GABAergic input recorded at different membrane compartments such as the soma . vs. the proximal dendrite. Our results suggest that GABAA receptor-mediated perisomatic input is massively activated during burst synchronization and that its kinetic properties and charge density are similar at the soma and proximal dendrite. These functional results match structural data published by other laboratories very well and strengthen the hypothesis that the potential preservation of perisomatic GABAergic input in intractable epilepsies may be a key factor in the generation of pathological network activity.
AB - Perisomatic GABAergic input appears spared or even increased in intractable temporal lobe epilepsy, and has been suggested to contribute to the generation of pathological discharges. Nevertheless, its degree of functional activity during epileptiform synchronization has not been thoroughly investigated. Thus, it remains unclear how structural preservation or loss of domain-specific GABAergic input may affect the network. Here, we have taken advantage of a model of epileptiform activity . in vitro to quantify the charge transfer provided by perisomatic GABAA receptor-mediated input to CA1 pyramidal neurons during interictal-like bursts. By recording both firing in GABAergic interneurons and the charge transfer generated by unitary postsynaptic currents to target pyramidal cells, we have estimated the charge transfer that would be dynamically generated by the recruitment of the entire pool of perisomatic-targeting interneurons and the number of perisomatic-targeting interneurons that would be required to generate the experimentally observed GABAergic input. In addition, we have recorded and compared the dynamics and charge density of GABAergic input recorded at different membrane compartments such as the soma . vs. the proximal dendrite. Our results suggest that GABAA receptor-mediated perisomatic input is massively activated during burst synchronization and that its kinetic properties and charge density are similar at the soma and proximal dendrite. These functional results match structural data published by other laboratories very well and strengthen the hypothesis that the potential preservation of perisomatic GABAergic input in intractable epilepsies may be a key factor in the generation of pathological network activity.
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U2 - 10.1113/jphysiol.2009.179945
DO - 10.1113/jphysiol.2009.179945
M3 - Article
C2 - 19840998
AN - SCOPUS:71249126631
SN - 0022-3751
VL - 587
SP - 5691
EP - 5708
JO - Journal of physiology
JF - Journal of physiology
IS - 23
ER -