29-30 January, 2020 - Szeged, Hungary


Abstract details

Physiological and pathological synchronies in the human neocortex, in vitro


Lucia Wittner1

1 Institute of Cognitive Neuroscience and Psychology, Research Center for Natural Sciences, Budapest, 2National Institute of Clinical Neuroscience, Budapest, 3Faculty of Information Technology and Bionics, Pázmány Péter Catholic University, Budapest

Most of the brain’s cognitive functions are based on neuronal synchronisation processes. Knowledge about the coordinated firing of neuronal populations is essential in understanding the generation mechanisms of physiological and pathological synchronies. In focal epilepsies, the human neocortex generates hypersynchronous convulsive activity between seizures, classified as interictal discharges. The initiation of these paroxysmal events has been linked to hyperexcitability and to bursting behaviour of neurons in animal models. Despite the importance of interictal spikes in epilepsy diagnostics, little is known about their cellular mechanisms in humans. We investigated spontaneously occurring physiological synchronous population activity and interictal-like spikes, as well as disinhibition-induced epileptiform activity in human neocortical slice preparations derived from epileptic and non-epileptic tumour patients. Physiological neocortical activity was characterised by the complex interactions of excitatory and inhibitory cells. Spontaneously emerging interictal-like discharges also involved both excitatory and inhibitory circuits, however, excitatory cells, and especially intrinsically bursting neurons had a leading role in the generation of these hypersynchronous events. In contrast, when GABAergic neurotransmission was reduced, both epileptiform interictal discharges and seizures were mainly initiated by the synchronous and intense discharge of inhibitory cells. Our data suggest the importance of the finely tuned balance of excitation and inhibition in the generation of physiological synchronisation, which is shifted towards an enhanced excitability in epilepsy. Furthermore, our results draw attention to the differences between acute pharmacological models and the human disease.