Upregulation of GABA receptor promotes long‑term potentiation and depotentiation in the hippocampal CA1 region of mice with type 2 diabetes mellitus

Type 2 diabetes mellitus (T2DM) is a long-term metabolic disorder characterized by high blood sugar levels, insulin resistance and a relative lack of insulin. A previous study has reported that an association exists between γ-aminobutyric acid (GABA) and the hippocampus. The current study therefore aimed to assess the effect of the GABA receptor (GABA-R) on the long-term potentiation (LTP) and depotentiation of the hippocampal CA1 region in mice with T2DM. Mice were divided into four groups: A normal group consisting of healthy mice and a GABA-R, negative control and blank group all comprising T2DM mice. The weight and blood glucose level of all mice were measured and GABA-R mRNA and protein expression were detected. A hydroxyl free radical (OH-) kit was used to determine the hippocampal OH-content. Using an electrophysiological experiment, the population spike (PS) slope was observed every 5 min. The results revealed that as GABA-R levels increased, the weight, blood glucose level and OH− content of the T2DM mice significantly decreased, and the neuron microstructures in the mice hippocampal tissue improved. The PS slope also significantly increased and the level of depotentiation improved. The results of the current study support the theory that the upregulation of GABA-R protects the neuronal ultrastructure and promotes LTP and depotentiation in the hippocampal CA1 region by inhibiting the accumulation of OH− in T2DM mice.