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. Author manuscript; available in PMC: 2020 Feb 9.
Published in final edited form as: Neuropharmacology. 2018 Jun 28;139:150–162. doi: 10.1016/j.neuropharm.2018.06.035

Figure 6. Intracellular Ca2+ stores were involved in mGluR-mediated slow oscillations.

Figure 6.

(A) Sample current trace showing that exposure to DHPG produced reduced membrane depolarization and slow oscillations in the presence of BAPTA. The Ca2+ chelator BAPTA (30 mM) was included in the pipette to clamp intracellular Ca2+ to lower levels. (B) Blockade of ryanodine receptors by ryanodine (10 μM) attenuated DHPG-mediated depolarization and slow oscillations. Slices were pre-incubated with ryanodine for 30 min before exposure to DHPG. (C) Population data revealed that the DHPG-induced depolarization was significantly attenuated by BAPTA (n=8, p<0.01), and ryanodine (n=10, p<0.001). (D) Population data showing that the number of oscillations were blocked by BAPTA (n=8, p<0.001) and ryanodine (n=10, p<0.001).