IBRO WORKSHOP

29-30 January, 2020 - Szeged, Hungary

 
 

Abstract details

QUANTITATIVE EXAMINATION OF PERISOMATIC INPUT TO PRINCIPAL NEURONS IN DYSGENETIC CORTICES OF HUMAN EPILEPTIC PATIENTS

01/29/2020

CECÍLIA PARACZKY1, PÉTER SZOCSICS1, LÓRÁND ERŐSS2, LUCA BARNAFÖLDI2, LASZLÓ HAVAS3, ZSÓFIA MAGLÓCZKY14

1 Human Brain Research Laboratory, Institute of Experimental Medicine, Budapest

2 National Institute of Clinical Neuroscience, Budapest 3St. Borbála Hospital, Tatabánya 4Laboratory of Cerebral Cortex, Institute of Experimental Medicine, HAS, Budapest

Keywords: FCD, Epilepsy The focal cortical dysplasia (FCD) is a neurodevelopmental disorder, often associated with drug resistant epilepsy disease. In the different FCD types several pathological changes can be found, such as abnormal cell types and cortical lamination. Type II FCDs are characterized by the presence of morphologically abnormal cell, including cytomegalic dysmorphic neurons or balloon cells and abnormal glial cells besides the different degree disruption of the cortical lamination. Dysmorphic neurons among others exhibit aberrant dendritic arborization, and markedly enlarged cell body, can be detected with SMI32 and NeuN immunostaining. Balloon cells are present specifically in type IIb (Taylor-type) FCDs, most of them can be detected with both mentioned (NeuN, SMI32), and with PV immunostaining also. The previous investigations of our group were performed on hippocampal surgical samples of patients with temporal lobe epilepsy, and enhanced perisomatic inhibition was found, which may increase synchronous firing of principal cells and seizure probability. Therefore, we wanted to investigate, whether changes of perisomatic inhibitory inputs can be found in epilepsy with FCD background, suggesting the possibility of similar patomechanism in different types of epilepsies. Surgical samples from FCD patients with drug resistant epilepsy (ILAE: FCD IIb, 6 cases: 4 frontal, 1 parietal, and 1 occipital cortex sample) were compared to controls of the same cortical regions with short post mortem interval (2-5 h) (6 control subjects: 4 samples from Br46, 1 from Br7, and 1 from Br18. Perisomatic input of cortical pyramidal cells was measured to reveal the potential abnormal inhibitory mechanism. Support: National Research, Development and Innovation Office of Hungary (grant K 125436) and National Brain Research Program (2017-1.2.1-NKP-2017-00002)