Fig. 1

STN–ANT plasticity is crucial for the motor control in Parkinson’s disease model. a Representative images of EYFP-positive fibers in ipsilateral ANT in coronal brain slices. n = 5 mice. Scale bar, 200 μm. b Representative images of EYFP-positive ANT cells stained with anti-CaMKII or -GABA antibodies. Short arrows pointed to the neurons co-labeled. Inset: magnified views of arrowhead regions. Scale bar, 200 μm. n = 5 mice. c Schematics for in vitro examination of the functional connection from STN to ANT (left). Representative trace of the evoked EPSC in ANT neurons in the presence of TTX and 4-AP (right). d Firing rate of neurons in contralateral and ipsilateral ANT of PD model rats. n = 11 rats. e Spectrogram and power spectrum density analysis of local field potentials in PD model rats. f Time of passing the beam and the number of APO-induced rotations in PD model mice with injection of solvent control (ascorbic acid, AA) or IBO in ipsilateral ANT (right). n = 6–7 mice in each group. g Schematics of optical stimulation (yellow bar, 590 nm, 4 s, continuous) of eNpHR-positive fibers from STN in ipsilateral ANT (top) and functional verification of eNpHR (bottom). n = 3 mice. h Time of passing the beam and the number of APO-induced rotations in PD model mice with the 590 nm optical stimulation on or off. n = 7–8 mice in each group. i AMPAR/NMDAR current ratio evoked by optical stimulation. n = 6–7 mice in each group. j Rectification index of AMPAR stimulated by optical stimulation in normal (Nor) and PD model mice. n = 6–7 mice in each group. k Western blot images and quantitative analysis of GluR1, GluR1-S831, H-89/GluR1-S831, GluR1-S845, H-89/GluR1-S845 using the extracts from contralateral (Con) or ipsilateral (Ips) ANTs of PD mice. n = 5–10 mice in each group. β-actin was used as a loading control. l AMPAR/NMDAR current ratio in ipsilateral ANT neurons evoked by electrical stimulation in the presence of aCSF or H-89 (left) (n = 3 mice) and time of passing the beam and the number of APO-induced rotations in PD model mice after infusion of H-89 into ANT (middle and right). n = 7–8 mice in each group for the behavioral test. m The number of APO-induced rotations in MPTP-PD model mice after infusion of H-89 into ANT. n = 9 mice. n AMPAR/NMDAR current ratio in ipsilateral ANT neurons in the presence of aCSF or TAT-S845 in PD model mice (left) (n = 3 mice) and time of passing the beam and the number of APO-induced rotations in PD model mice after infusion of TAT-S845 into ANT (middle and right). n = 7–8 mice in each group for the behavioral test. o Schematic shows the strengthen of synaptic plasticity in STN–ANT circuit resulted from increased PKA phosphorylation of GluR1-S845 in PD models and which in turn play a critical role in PD motor deficits. In d, i, j, l (left), n (left) each circle represents a neuron, and in f, h, k, l (middle and right), m, n (middle and right) each circle represents a mouse. Mann–Whitney test was used for analysis of firing rates from in vivo recording. The other data were analyzed by Student’s t test. Data are presented as mean ± SEM of at least three independent experiments, except firing rates from in vivo recording (d) which were presented as median (interquartile range)