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. 2017 Jul 26;37(30):7140–7148. doi: 10.1523/JNEUROSCI.0876-17.2017

Figure 3.

Figure 3.

Combined antagonism of GABAARs and KORs blocks heterosynaptic suppression of HP inputs in the VS. A, Group data of HP and PFC EPSP amplitudes averaged over 5 min. Bath application of U69,593 (1 μm) significantly reduced the amplitude of HP- and PFC-evoked responses. Black bar represents the duration of drug application. B, Plot comparing EPSP amplitudes evoked by HP stimulation under baseline and U69,593 conditions for individual MSNs. Values represent the average of the last 5 min of baseline compared with the last 5 min of the recording session (and in Fig. 4). Inset, Representative EPSPs evoked under baseline (black) and U69,593 conditions (green) are overlaid. Open black symbols represent corresponding data. Closed black symbols represent group averages. C, Plot comparing EPSP amplitudes evoked by single-pulse PFC stimulation under baseline and U69,593 conditions. D, Averaged EPSP amplitudes for individual MSNs treated with norBNI (100 nm) showing that HP2 EPSPs are still significantly reduced compared with HP1 responses evoked at a similar membrane potential. Inset, Averaged depolarized HP1 and basal HP2 EPSPs in the same representative cell. E, Plot comparing the magnitude of HP2 suppression driven by PFC stimulation under baseline conditions and in the presence of norBNI for individual MSNs. Blockade of κ opioid receptors reduced the extent of HP2 heterosynaptic suppression induced by PFC stimulation. F, Responses to optogenetic stimulation of HP terminals before (HP1) and 50 ms after (HP2) PFC train stimulation in a representative MSN treated with norBNI. Inset, Averaged responses to HP1 and HP2 (highlighted in red and blue, respectively) are overlaid (average of 15 sweeps; gray). G, Averaged EPSP amplitudes for individual MSNs treated with norBNI (100 nm) and PTX (100 μm) showing that HP1 and HP2 responses do not differ compared at a similar membrane potential. H, Plot comparing the magnitude of HP2 suppression driven by PFC stimulation under baseline conditions and in the presence of norBNI and PTX for individual MSNs. Blockade of GABAARs and KORs reversed the heterosynaptic suppression of HP2 responses by PFC stimulation. I, Responses to optogenetic stimulation of HP terminals before (HP1) and 50 ms after (HP2) PFC train stimulation in a representative MSN treated with norBNI and PTX. *p < 0.05.