Skip to main content
. Author manuscript; available in PMC: 2024 May 13.
Published in final edited form as: Cell Rep. 2024 Mar 2;43(3):113834. doi: 10.1016/j.celrep.2024.113834

Figure 6. GABAAR autoinhibition of phasic DA release persists when effects of glutamate co-release or nAChR activation are prevented, confirming direct action by co-released GABA.

Figure 6.

(A) In the dStr, PTX (100 μM) continued to produce a greater enhancement of 10 p- versus 1 p-evoked [DA]o in the presence of a mGluR1 antagonist (JNJ-16259685, 10 μM) and significantly increased the ratio of phasic (10 p) to tonic (1 p) DA signaling (n = 6 mice, paired t test).

(B) In the NAc core, greater enhancement of 10 p- versus 1 p-evoked [DA]o with PTX persisted in a cocktail of antagonists for AMPARs (DNQX, 10 μM) and NMDARs (D-AP5, 50 μM), as did the increased ratio of phasic-to-tonic DA release (n = 6 mice, paired t test).

(C) In the dStr, PTX continued to produce a greater enhancement of 10 p- versus 1 p-evoked [DA]o in the presence of a nAChR antagonist (DHβE, 1 μM) and significantly increased the ratio of phasic (10 p) to tonic (1 p) DA signaling (n = 6 mice, paired t test).

**p < 0.01, ***p < 0.001 versus respective 1 p stimulation or control (paired t tests) in males (blue circles) plus females (orange circles). Data are mean ± SEM.