Fig. 3: Chemogenetic inhibition of PV+ neurons in audTRN impairs PPI performance.
From: Involvement of the thalamic reticular nucleus in prepulse inhibition of acoustic startle
A Strategy of chemogenetic inhibition of PV+ neurons in audTRN. A Cre-dependent AAV for expression of hM4Di was bilaterally injected into the audTRN in PV-cre mice. B Left, example of confocal image showing overlap of hM4Di+ neurons (red, right) and PV+ neurons (green, middle). White dotted lines mark the border of the audTRN. Scale bar: 100 µm. C Quantification shows that approximately 89.41% of hM4Di cells are PV+ (N = 9 slices of 3 mice). D Left, schematic of experiment design. Right, a representative trace recorded in current-clamp mode from an audTRN PV neuron that expressed hMD4i. Scale bars: 1 min, 20 mV. Application of CNO (5 µM) abolished neuronal firing. E, F Application of CNO (3 mg/kg, i.p.) to mice that expressed hMD4i in audTRN PV neurons had no effect on total distance in OFT (Student’s t-test, t22 = 0.1871, P = 0.8533, N = 12 mice per group) or startle reflex in PPI (Student’s t-test, t23 = 0.0559, P = 0.9559, NmCherry = 11 mice, NhM4Di = 14 mice). G Application of CNO (3 mg/kg) to mice that expressed hMD4i in audTRN PV neurons impaired PPI performance (two-way ANOVA, F(1,165) = 18.90, P < 0.0001, NmCherry = 16 mice, NhM4Di = 19 mice). ****P < 0.0001.
