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. Author manuscript; available in PMC: 2022 Sep 1.
Published in final edited form as: J Neurogenet. 2021 Jun 7;35(4):358–369. doi: 10.1080/01677063.2021.1931180

Figure 4. Excessive D1-PKA signaling underlies cocaine-induced impairment of mGluR1-LTD.

Figure 4.

A. Co-application of SCH23390 (SCH, 10 μM) in the bath restored DHPG-LTD in slices prepared from cocaine mice. N = 8 cells from 8 mice.

B. Administration of SCH23390 in vivo restored DHPG-LTD in cocaine-treated mice. SCH23390 (1mg/kg, IP) was injected 30 min before mice were sacrificed for recording. N = 7 cells from 5 mice.

C. Inclusion of PKI 6-22 (PKI, 20 μM) in the patch pipette fully restored DHPG-LTD in cocaine mice. N = 6 cells from 3 mice.

D. Co-application of SKF81297 (2 μM) in the bath failed to block DHPG-LTD in saline mice. N = 7 cells from 4 mice. All recordings were performed on slices derived from mice treated with 7-day cocaine or saline injections followed by 1 day of withdrawal.