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Results: 5

1.
Fig. 3.

Fig. 3. From: ?-Opioid Receptors Selectively Regulate Basal Inhibitory Transmission in the Central Amygdala: Lack of Ethanol Interactions.

Baseline activities of spontaneous IPSCs in CeA neurons from MOR KO and WT mice. A, representative traces of spontaneous IPSCs from WT (top) and MOR KO (bottom) mice. Top two traces of spontaneous IPSCs are in the absence of TTX (sIPSCs), and bottom two traces are in the presence of TTX (mIPSCs). B, averaged cumulative fraction plots of frequency (left) and amplitudes (right) of sISPCs (top) and mIPSCs (bottom). Insets, mean frequency and amplitudes, respectively, from WT mice (open columns) and MOR KO mice (closed columns). MOR KO mice show greater baseline frequency of both sIPSCs and mIPSCs and greater baseline amplitude of sIPSCs; *, p < 0.05. Amplitude of mIPSCs was not significantly different (NS).

Maeng-Hee Kang-Park, et al. J Pharmacol Exp Ther. 2009 January;328(1):284-293.
2.
Fig. 5.

Fig. 5. From: ?-Opioid Receptors Selectively Regulate Basal Inhibitory Transmission in the Central Amygdala: Lack of Ethanol Interactions.

Ethanol effects on mIPSCs in CeA neurons from MOR KO and WT mice. A and B, representative mIPSCs before and during ethanol treatment and after washout of ethanol in CeA neurons from WT (A) and MOR KO (B) mice. C, cumulative plot of mIPSC frequencies before and during ethanol treatment from WT (left) and MOR KO (right) mice. In both groups, ethanol moved the cumulative frequency plot to the left by a comparable relative magnitude. D, averaged frequency and amplitudes, respectively, from WT mice (open columns) and MOR KO mice (closed columns). Ethanol increased the frequency of mIPSCs without significant changes in amplitude in both groups, suggesting increased vesicular GABA release in both cases; *, p < 0.05.

Maeng-Hee Kang-Park, et al. J Pharmacol Exp Ther. 2009 January;328(1):284-293.
3.
Fig. 2.

Fig. 2. From: ?-Opioid Receptors Selectively Regulate Basal Inhibitory Transmission in the Central Amygdala: Lack of Ethanol Interactions.

Baseline activities of evoked GABAergic synaptic responses in CeA from MOR KO and WT mice. Inhibitory synaptic responses were examined in current-clamp (A and B) and voltage-clamp (C) modes. The IPSPs and IPSCs were evoked at five different stimulus intensities. Open circles, WT mice; closed circles, MOR KO mice. Insets, representative traces. For equivalent stimulus intensities, amplitudes of evoked IPSPs and IPSCs from MOR KO mice were greater than WT mice. B, paired-pulse ratios of IPSPs were evoked at interpulse intervals of 50 and 100 ms. For both intervals, the paired-pulse ratios were less in MOR KO mice than in WT mice, suggesting that the difference in the magnitude of IPSP amplitudes could be because of presynaptic effects resulting in enhanced GABA release in the CeA of MOR KO mice; *, p < 0.05.

Maeng-Hee Kang-Park, et al. J Pharmacol Exp Ther. 2009 January;328(1):284-293.
4.
Fig. 1.

Fig. 1. From: ?-Opioid Receptors Selectively Regulate Basal Inhibitory Transmission in the Central Amygdala: Lack of Ethanol Interactions.

Effects of MOR activation on IPSCs in mice CeA neurons. A, representative current traces of mIPSCs before (Control), during application of DAMGO (1 μM) and after washout (Wash). B, representative current traces with the MOR-specific antagonist naloxonazine (1 μM). C and D, traces of averaged mIPSCs. There were no differences in the amplitude of mIPSCs with either drug. E and F, averaged cumulative fraction plots of mIPSC frequency. DAMGO shifts the mIPSC cumulative frequency plot to the right (E), whereas naloxonazine shifts the mIPSC frequency plot to the left without changes in amplitude (F), suggesting a tonic effect of MOR activation on vesicular GABA release. G, effect of naloxonazine (1 μM) on evoked IPSCs in mouse CeA neurons. Time course of mean IPSC amplitude changes, with representative traces taken before and during 1 μM naloxonazine at the corresponding numbered time points shown on the left. H, effect of DAMGO and naloxonazine on mean IPSC amplitudes compared with baseline. The DAMGO effect was abolished when slices were pretreated with naloxonazine; *, p < 0.05.

Maeng-Hee Kang-Park, et al. J Pharmacol Exp Ther. 2009 January;328(1):284-293.
5.
Fig. 4.

Fig. 4. From: ?-Opioid Receptors Selectively Regulate Basal Inhibitory Transmission in the Central Amygdala: Lack of Ethanol Interactions.

Ethanol effects on evoked GABAergic synaptic responses in CeA neurons from MOR KO and WT mice: effects on IPSPs in current-clamp mode (A and B) and on IPSCs in voltage-clamp mode (C). A, ethanol effects on IPSPs were not significantly different (by ANOVA) between WT and MOR KO mice over five different stimulus intensities. B, representative traces before (baseline), during ethanol treatment (ethanol), and after ethanol washout (washout). C, ethanol effects on paired-pulse ratios of IPSPs evoked at a stimulus intensity giving a 50 to 60% maximal response for the primary IPSP, with interpulse intervals of 50 and 100 ms. Ethanol decreased the paired-pulse ratio at both intervals, suggesting presynaptic effects (increased GABA release). However, the magnitude of changes in the paired-pulse ratio was not significantly different between WT and MOR KO mice. D, representative traces before (baseline), during ethanol treatment, and after ethanol washout. E, ethanol effects on evoked IPSCs in whole-cell patch showing time course of responses in CeA from WT and MOR KO mice. F, representative IPSC traces before (1), during ethanol treatment (2), and after ethanol washout (3). Scaled traces demonstrate no change in the kinetics of the IPSCs. G, mean percentage change in the amplitude of evoked IPSCs in the presence of ethanol. Ethanol increased the amplitudes of evoked IPSCs in CeA neurons from WT and MOR KO mice without a significant difference in the magnitude of ethanol effects between WT and MOR KO mice; *, p < 0.05.

Maeng-Hee Kang-Park, et al. J Pharmacol Exp Ther. 2009 January;328(1):284-293.

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