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. 2014 Jul 30;34(31):10247–10255. doi: 10.1523/JNEUROSCI.1680-14.2014

Figure 6.

Figure 6.

Expressing ASIC1A in the BNST is sufficient to increase CO2-evoked freezing. A, ASIC1A immunofluorescence in the BNST (white) of Asic1a−/− mice injected with AAV-ASIC1A. B, ASIC1A immunofluorescence in the dorsal hippocampus (white) of Asic1a−/− mice injected with AAV-ASIC1A. C, Whole-cell voltage-clamp recordings of neurons from BNST slices. AAV-ASIC1A produced acid-evoked currents in the BNST of Asic1a−/− mice. D, Quantification of freezing evoked by 10% CO2 in mice of indicated genotypes, viruses, and injection sites. In Asic1a−/− mice, AAV-ASIC1A in the BNST significantly increased freezing relative to AAV-eGFP injected controls, whereas AAV-ASIC1A in dorsal hippocampus (Hipp) did not. In Asic1a+/+ mice, AAV-ASIC1A in the BNST significantly increased CO2-evoked freezing relative to AAV-eGFP controls. E, Infusion of AAV-ASIC did not alter locomotion in the open field.