Fig. 5: Inhibition of GABAB receptor prevents rebound bursting in the MG and impairs PPI performance.
From: Involvement of the thalamic reticular nucleus in prepulse inhibition of acoustic startle
A Electrophysiological recording in MG slice of PV-cre: Ai14 mice. A stimulating electrode was placed in the audTRN fiber path. The electrical stimulation frequency was 300HZ. B Left, example of burst firing induced by electrical stimuli of the inhibitory audTRN–MG pathway. 100 μM APV and 20 μM CNQX were used to block excitatory input. The amplitude of hyperpolarization was calculated between two dotted horizontal lines. Right, enlarged trace from the dotted line area in the left trace. Scale bars: 100 ms, 10 mV. C Example trace of rebound burst firing without drug treatment (left, groupcontrol), with GABAA receptor antagonist 20 μM BMI treatment (middle, blue, groupBMI), or with GABAB antagonist 0.5 μM CGP55845 treatment (right, red, groupCGP). D, E Hyperpolarization and rebound burst firing were blocked by GABAB receptor antagonist but not by GABAA antagonist (D amplitude of hyperpolarization, groupcontrol versus groupCGP, Student’s t-test, t7 = 10.110, P < 0.0001; E number of burst firing, groupcontrol versus groupCGP, Mann–Whitney two-tailed t-test, P = 0.0079, N = 5 cells). F Schematic of pharmacology experiment. Cannulas were unilaterally implanted into MG of C57 mice. After 7 days recovery, mice were given 0.1 mM CGP55845 or ACSF 30 min before OFT and PPI paradigm. G, H Infusion of 0.1 mM CGP55845 to MG of mice had no effect on total distance in OFT (Student’s t-test, t17 = 0.103, P = 0.9190, NACSF = 9 mice, NCGP = 10 mice) or startle reflex in PPI (Student’s t-test, t16 = 0.834, P = 0.4163, NACSF = 8 mice, NCGP = 10 mice). I Infusion of 0.1 mM CGP55845 to MG of mice impaired PPI performance (two-way ANOVA, F(1,80) = 8.733, P = 0.0041, NACSF = 8 mice, NCGP = 10 mice). **P < 0.01,****P < 0.0001.
