Laboratory of Epileptogenesis

Head: Katarzyna ŁUKASIUK

Staff: Joanna Bednarczyk (PhD student), Anna Bot (PhD student), Konrad Dębski, Diana Miszczuk (PhD student), Dorota Nowicka, Elżbieta Wiernasz

Research profile:

Our research is concentrated on the molecular responses to brain injury and molecular events leading to the develop- ment of epilepsy. We are particularly interested in alterations in gene expression that lead to the development of spon- taneous seizures in in vivo models of epileptogenesis and epilepsy. We are also interested in developing new strate- gies to prevent epilepsy development

Methods:

• animal models of epileptogenesis and epilepsy
• video-EEG monitoring
• neuronal cell cultures
• gene silencing and overexpresssion in neurons in vitro
• in situ hybridization
• RT-PCR
• immunohistochemistry
• immunocytochemistry
• immunoblotting
• basic molecular biology methods

Current research activities:

• search for new genes involved in development of epilepsy
• the role of Ttyh1 in normal brain and in brain pathology
• investigation of compounds influencing immune system as a potential drugs for modification of epileptogenesis and epilepsy
• role of neurogenesis in epileptogenesis and epilepsy

Selected publications:

Guzik-Kornacka A., Śliwa A., Plucińska G., Łukasiuk K. (2011) Status epilepticus evokes prolonged increase in the expression of CCL3 and CCL4 mRNA and protein in the rat brain. Acta Neurobiologiae Experimentalis (Wars), 71: 193-207.

Łukasiuk K., Wilczyński G.M., Kaczmarek L. (2011) Extracellular proteases in epilepsy. Epilepsy Research, 96: 191-206.

Pitkänen A., Łukasiuk K. (2011) Mechanisms of epileptogenesis and potential treatment targets. The Lancet Neurology, 10:
173-186.

Stefaniuk M, Świech L, Dzwonek J, Łukasiuk K. (2010) Expression of Ttyh1, a member of the Tweety family in neurons in vitro and in vivo and its potential role in brain pathology. Journal of Neurochemistry, 115: 1183-1194.

Śliwa A., Plucińska G., Bednarczyk J., Łukasiuk K. (2012) Post-treatment with rapamycin does not prevent epileptogenesis in the amygdala stimulation model of temporal lobe epilepsy. Neuroscience Letters, 509: 105-109