Acupressure Potentially Promoting the Learning and Memory Capabilities of Hypoxic Ischemic Cerebral Palsy Rats

Whether acupressure could improve the learning and memory capabilities in hypoxic-ischemic cerebral palsy (HIE) in rats and whether the mechanism is related to hippocampal neuroplasticity were investigated.

In this study, we used a unilateral HIE rat model. There were three groups, including the sham control group, the HIE control group, and the acupressure group. The acupressure group was given a 4-week treatment after the HIE modeling. The learning and memory ability of rats was tested by the open field, novel object recognition (NOR), Y maze, and Morris water maze (MWM) behavioral experiments. The hippocampal spine density and dendrites' branch number and length were detected using Golgi staining. The thickness, width, and length of pre- and postsynaptic membranes were observed using electron microscopy. The postsynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunits AMPAR1, AMPAR2, and N-methyl-D-aspartate receptor 2B (NMDAR2B) were visualized by immunohistochemistry and immunofluorescence staining. The brain neuron electrical activity at the rat hippocampal CA1 region was recorded by awake electroencephalography (EEG). Furthermore, the AMPAR and N-methyl-D-aspartate receptor (NMDAR) protein expression in the hippocampus was detected using western blot.

Acupressure could alleviate HIE-induced behaviors and promote the recovery of neural plasticity functions in the hippocampus, showing the broading of the synaptic cleft, improving the synaptic membrane, increasing dendrites' branch numbers, prolonging the length of the dendrites, and enhancing the spine density (p < 0.05). The neural plasticity-related proteins in the hippocampus, including AMPAR and NMDAR, were all downregulated in the HIE group (p < 0.05). Immunofluorescence staining results displayed the same trend in terms of the NMDAR and AMPAR positivity rate (p < 0.05). However, these effects could be partly reversed after being treated by acupressure (p < 0.05). As for the EEG results, the spectrum became slow-wave (increased δ and decreased θ) with disordered amplitudes in the model group, reflecting neuronal damage, while the spectrum partially recovered (θ rebounded and δ decreased) in the treatment group, suggesting the effectiveness of the intervention.

Acupressure can ameliorate the learning and memory function of HIE by regulating the mechanism related to postsynaptic membrane, promoting the recovery of functional plasticity and neural plasticity-related electric signal upregulation in the hippocampus.