Kim KM, Tercan S, Baday M, Mahaney KB, Recht LD, Rajadas J, and Patel CB
2021 10th International IEEE/EMBS Conference on Neural Engineering (NER)
Glioma tumors originate from glial cells in various locations in the nervous system, including the brain and spinal cord. Gliomas express neurotransmitter receptors that can increase neuronal excitability via excitatory or inhibitory pathways which can result in brain tumor-associated epilepsy (BTAE), as well as form synapses with neurons to drive their own growth. In this study, the authors hypothesized that isolated glioma may their own characteristic electrophysiological response to drugs known to affect neural synaptic activity. A multiwell microelectrode array (MEA) system was used to observe neural field potentials and measure mean firing rate (MFR) from glioma spheroids in the absence or presence of pro-seizure and anti-seizure drugs. Pro-seizure drugs, pentylenetetrazole (PTZ) and AMPA, signficantly increased the MFR of glioma spheroids over baseline b either blocking inhibitory GABA receptors or stimulating AMPA receptors, respectively. In contrast, the anti-seizure drugs, tiagabine (TIAG) and perampaenl (PER), had no effect on MFR, suggesting that glioma spheroid electrophysiology may only be modulated by pro-seizure drugs or that anti-seizure drug affect may be dependent on the frequency of synaptic activity prior to dosing. Future studies will focus on further characterizing the glioma electrical activity by investigating synaptic connectivity and network within glioma spheroids and between glioma and other neural cell types.