• Li Yang, De Wu, Baotian Wang, Xiaosong Bu, Jing Zhu, and Jiulai Tang.
• Department of Paediatrics, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
• Arch Med Sci. 2020 Jan 1; 16 (1): 200204200-204.

IntroductionThe aim of our study is to investigate the effect of hyperbilirubinaemia on synaptic plasticity in the dentate gyrus (DG) region of the rat hippocampus.Material And MethodsSeven-day-old healthy Sprague Dawley (SD) rats were randomly divided into a control group and an experiment group (n = 20 in each group). The input/output (I/O) functions, paired-pulse reactions (PPR), excitatory postsynaptic potential (EPSP), and population spike (PS) amplitude were measured in the DG area of both groups of rats in response to stimulation applied to the lateral perforant path.ResultsCompared with that in the control rats, the current-voltage curves of both EPSP slope and PS amplitude in the experimental rats were significantly depressed. The average peak facilitation was 187 ±16% in the control and 164 ±18% in the experiment group (F = 21.054, p < 0.01). The facilitation period duration of PS was 155 ms in the experimental rats, which was less than that of the controls (235 ms). In the control group, the long-term potentiation (LTP) amplitudes were 140 ±3.5% and 242 ±6%, when estimated from the EPSP slope and PS amplitude, respectively, which were significantly depressed to 124 ±3.4% (EPSP slope, F = 70.489, p < 0.01) and 138 ±8.6% (PS amplitude, F = 253.46, p < 0.01), respectively, in the experiment group.ConclusionsThese findings suggest that hyperbilirubinaemia could induce impairment of synaptic plasticity in the rat DG area in vivo, including I/O function, paired-pulse ratio (PPR), and LTP, which may be closely related to cognitive impairment.Copyright: © 2019 Termedia & Banach.

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