Skip to main content
. Author manuscript; available in PMC: 2022 Oct 1.
Published in final edited form as: Mol Neurobiol. 2021 Jun 26;58(10):4787–4801. doi: 10.1007/s12035-021-02461-3

Fig 2.

Fig 2

No change in basal dopamine and cannabinoid tone or inhibitory plasticity in MSNs in NAc core but change in inhibitory transmitter release probability. A. Application of D1 receptor antagonist SCH23390 (10 μM) reduced the amplitude and frequency of mIPSC from MSNs in NAc core. Similar extent of reduction in mIPSC characteristics were observed in both wildtype and GluD1 KO (N = 6 from 3 animals per genotype). B. CB1 receptor inverse agonist (rimonabant) did not affect mIPSCs in both wildtype and GluD1 KO suggesting no change in basal endocannabinoid tone (N = 5–7 from 3 animals per genotype). C. Evoked paired-pulse IPSC responses were obtained from MSNs in NAc core. Application of CB1 agonist CP55940 (2 μM) reduced the evoked IPSC response in both wildtype and GluD1 KO MSNs to similar extent (N = 10–11 from 3 animals per genotype). D. Significantly higher baseline paired-pulse ratio of the IPSC was observed in GluD1 KO (WT: 0.8284 ± 0.02757 vs. GluD1 KO: 0.9891 ± 0.04632, p = 0.0066; Unpaired t-test)