Biology subjects

Tabatabaee, M. S.

Publications and source records attributed to Tabatabaee, M. S..

2 recordsLinked to original sources

bioRxiv2021

Aminooxadiazolyl kainic acid reveals that kainic acid receptors contribute to astrocytoma glutamate signaling

The excitatory neurotransmitter glutamate triggers a Ca2+ rise and the extension of processes in astrocytes. Our results suggest that kainic acid receptors (KAR) can independently initiate glutamate signaling in astrocytoma U118-MG cells. The natural product kainic acid triggered glioexcitablity in cells and was inhibited by the KAR antagonist CNQX, but its activity was lower than glutamate on KARs. We created a new heteroaryl kainoid based on rational design: aminooxadiazolyl kainic acid 1 (AODKA). AODKA induced a larger calcium influx and a faster processes extension than kainic acid in U118-MG cells. AODKA is a new tool to study KAR activity in the nervous system. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=145 SRC="FIGDIR/small/426948v1_ufig1.gif" ALT="Figure 1"> View larger version (27K): org.highwire.dtl.DTLVardef@1b63f72org.highwire.dtl.DTLVardef@1ff92c4org.highwire.dtl.DTLVardef@1fcb212org.highwire.dtl.DTLVardef@10ed76e_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2019

L-type voltage-gated calcium channel modulators inhibit glutamate-induced morphology in astrocytoma cells

The excitatory neurotransmitter glutamate evokes physiological responses within the astrocytic network that lead to fine morphological dynamics. However, the mechanism by which astrocytes couple glutamate sensing with cellular calcium rise remains unclear. Employing natural properties of U118-MG astrocytoma cells, we tested a possible connection between L-type voltage-gated calcium channels (Cav) and glutamate receptors. Using live confocal imaging and pharmacological inhibitors, the extension of U118-MG processes upon glutamate exposure are shown to depend mainly on extracellular calcium entry via L-type Cavs. Inhibitors of the Cav 1 protein, decreased astrocytic filopodia extension; while, gabapentinoids, ligands of the Cavs 2{delta} auxiliary subunit blocked all process growth. This study suggests that 2{delta} is the main contributor to Cavs role in glutamate-dependent filopodiagenesis. It opens new avenues of research on the role of 2{delta} in neuron-astrocyte glutamate signaling and neurochemical signaling at tripartite synapses.

neuroscience↗