Team Bosmans
Prof. Dr. Frank Bosmans
Dr. Rita De Cássia Collaço
Dr. Alessio Lissoni
Jolien De Waele
“As part of my PhD project, I am focusing on ligand-gated GABAA receptors which are linked to West syndrome (WS), a severe form of infantile epilepsy diagnosed in 1 in 3500 children. To investigate whether GABAA receptor mutations seen in WS patients dampen inhibitory transmission, I perform electrophysiological recordings on Xenopus oocytes (TEVC), HEK293 T cells, hippocampal neurons and brain slices. Our work has the potential to contribute new conceptual insights into the role of GABAA receptors in infantile spasms and can directly affect patient lives. As part of a side project, I also investigate voltage-gated Na+ channel β1 subunit mutations seen in patients with Generalized Epilepsy with Febrile Seizures (GEFS+) and Early Infantile Epileptic Encephalopathy (EIEE). The functional consequences of these mutations are investigated on NaV1.1, NaV1.2 and NaV1.6, the three most abundantly expressed NaV channels in the human brain. “
Wayra Backx
“The somatosensory nervous system perceives and transfers sensory modalities such as pain, itch, and temperature sensitivity from the periphery to the sensory cortex in the brain. Pain has been and continues to be extensively researched, whereas itch remains unjustifiably overlooked. Previous research has implicated voltage-gated sodium channel (Nav) 1.9 in pain-related syndromes as well as severe pruritis that leads to excessive scratching. My goal as a PhD student in the MPNG lab is to uncover the role of Nav1.9 in sensory perception through electrophysiological, behavioral and histological analyses of knock-out, gain-of-function and wild-type mice. To obtain electrophysiological data, I perform the patch clamp technique on spinal cord slices and neurons of dorsal root ganglia. In addition to my main project, I also explore the contribution of the Nav β4 subunit to resurgent currents, the expression and function of Nav1.9 in the sympathetic nervous system (SNS) and Nav implications in Primary Focal Hyperhidrosis and other SNS-related syndromes.” As part of a side project, I also investigate voltage-gated Na+ channel β1 subunit mutations seen in patients with Generalized Epilepsy with Febrile Seizures (GEFS+) and Early Infantile Epileptic Encephalopathy (EIEE). The functional consequences of these mutations are investigated on NaV1.1, NaV1.2 and NaV1.6, the three most abundantly expressed NaV channels in the human brain. “
Margaux Theys
” Voltage-gated sodium channels play a vital role in the perception of pain, since they rapidly transduce afferent stimuli in the skin to the spinal cord and the brain. Although several sodium channel subtypes have been associated with severe pain disorders, the NaV1.9 subtype is by far the most elusive. For my PhD, I am investigating the peculiar electrophysiological properties of NaV1.9 in heterologous expression systems as well as isolated dorsal root ganglionic neurons. Furthermore, we aim to elucidate the molecular pathways that influence NaV1.9 expression and gating, and relate this to in vivo pain experience using validated mouse behavioral assays. As such, we hope to gain insights in pain signaling on a molecular and integrative level, and consequently, lay the foundation for future drug development efforts. In addition to my main project, I also explore the contribution of the Nav β4 subunit to resurgent currents, the expression and function of Nav1.9 in the sympathetic nervous system (SNS) and Nav implications in Primary Focal Hyperhidrosis and other SNS-related syndromes.” As part of a side project, I also investigate voltage-gated Na+ channel β1 subunit mutations seen in patients with Generalized Epilepsy with Febrile Seizures (GEFS+) and Early Infantile Epileptic Encephalopathy (EIEE). The functional consequences of these mutations are investigated on NaV1.1, NaV1.2 and NaV1.6, the three most abundantly expressed NaV channels in the human brain. “
Maxime Lammens
Jolien Vander Cruyssen
Sara Cottyn
Lies Vancraeynest
