Protective effects of calcium ions via L-type calcium channels and NMDA receptors on prostaglandin E 2 -induced apoptosis in rat cortical cells

• Published in: Molecular biology reports Vol. 48; no. 5; p. 4517
• Main Authors: Uema, Shota, Horita, Mizue, Takadera, Tsuneo
• Format: Journal Article
• Language: English
• Published: Netherlands 01.05.2021
• Subjects: Animals; Apoptosis - drug effects; Calcium - metabolism; Calcium Channel Agonists - pharmacology; Calcium Channels, L-Type - metabolism; Calcium Signaling - drug effects; Carbazoles - pharmacology; Cells, Cultured; Cerebral Cortex - cytology; Cerebral Cortex - embryology; Dinoprostone - pharmacology; Enzyme Inhibitors - pharmacology; Ions - metabolism; N-Methylaspartate - pharmacology; Neurons - drug effects; Neurons - metabolism; Protective Agents - pharmacology; Protein Kinase C - antagonists & inhibitors; Pyrroles - pharmacology; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate - agonists; Receptors, N-Methyl-D-Aspartate - metabolism; Prostaglandin E2; L-type calcium channel; NMDA receptor; Apoptosis
• ISSN: 1573-4978
• DOI: 10.1007/s11033-021-06472-0

Calcium ions mediate a variety of physiological responses of developing neurons including survival. The purpose of this study was to examine the effect of calcium influx through L-type calcium channels (LTCCs) or NMDA receptors on prostaglandin E (PGE )-induced apoptosis in rat cortical cells. Cultures of rat cortical cells were prepared from an embryonic day 18 rat neocortex. After culturing for 2 or 8 days in vitro (DIV), the cells were subjected to PGE treatment for 48 h. FPL64176, an LTCC agonist, protected the cells at 2 and 8 DIV from PGE -induced apoptosis. On the other hand, N-methyl-D-aspartate (NMDA), an agonist of NMDA receptor, protected the cells from PGE -induced apoptosis only at 8 DIV. FPL64176 increased the calcium levels at 2 and 8 DIV, whereas NMDA increased the calcium levels only at 8 DIV. The protective effects of the LTCC agonist and NMDA on PGE -induced apoptosis were blocked following treatment of the cells with protein kinase C inhibitors. Our results suggest that LTCCs and NMDA receptors modulate the cell death of developing cortical neurons possibly through a protein kinase C pathway.