Fig. 4: NiCl2 causes blockage of burst firing of PV+ neurons in audTRN and PPI performance impairment.
From: Involvement of the thalamic reticular nucleus in prepulse inhibition of acoustic startle
A Electrophysiological recording in audTRN slice of PV-cre: Ai14 mice. B Left, example of burst firing induced by 60 pA inward current injection. Middle, action potential was blocked by 1 µM TTX. The spike between two dotted lines was T-type calcium channel spike, which was suppressed by 1 mM NiCl2 (right). Scale bars: 10 ms, 10 mV. C Burst firing was blocked by 1 mM NiCl2. D Quantification of the calcium spike amplitude from the TTX and TTX + NiCl2 group. NiCl2 blocked the calcium spike (paired two-tailed t-test, t4 = 31.390, P < 0.0001, N = 5 cells). E Quantification of the burst number from the control and NiCl2 group. NiCl2 blocked burst firing completely (paired two-tailed t-test, t4 = 6.000, P = 0.0039, N = 5 cells). F Schematic of pharmacological experiment. Cannulas were unilaterally implanted into audTRN of C57 mice. After 7 days recovery, mice were given 6 mM NiCl2 or ACSF 30 min before OFT and PPI paradigm. G, H Infusion of 6 mM NiCl2 into audTRN of mice had no effect on total distance in OFT (Student’s t-test, t22 = 0.5074, P = 0.6169, N = 12 mice per group) or startle reflex in PPI (Student’s t-test, t22 = 1.027, P = 0.3158, N = 12 mice per group). I Infusion of 6 mM NiCl2 into audTRN of mice impaired PPI performance (two-way ANOVA, F(1,110) = 14.480, P = 0.0002, N = 12 mice per group). **P < 0.01, ***P < 0.001, ****P < 0.0001.
