High sucrose consumption induces memory impairment in rats associated with electrophysiological modifications but not with metabolic changes in the hippocampus - Lemos, C.; Rial, D.; Gonçalves, F.Q.; Pires, J.; Silva, H.B.; Matheus, F.C.; da Silva, A.C.; Marques, J.M.; Rodrigues, R.J.; Jarak, I.; Prediger, R.D.; Reis, F.; et al. (Neuroscience, 2016)
Keywords: Adenosine; Animals; Diet - adverse effects; Dietary Sucrose - toxicity; Disease Models, Animal; Emotions - physiology; Helplessness, Learned; hippocampus; Hippocampus - physiopathology; Locomotion - physiology; Long-Term Potentiation - physiology; Long-Term Synaptic Depression - physiology; Male; memory; Memory Disorders - etiology; Memory Disorders - physiopathology; Motor Activity - physiology; Neurology; Rats, Wistar; Receptor, Adenosine A1 - metabolism; Recognition (Psychology) - physiology; sucrose; Synapses - physiology; synaptic plasticity; Synaptic Transmission - physiology; A1R; Adenosine; memory; hippocampus; DMSO; FST; T2D; HRMAS; LTP; HSu; PP-LFS; sucrose; TA; NAA; NOR; fEPSP; OD; OF; GABA; synaptic plasticity; DPCPX; LTD; EC; adenosine A 1 receptors; high-resolution magic angle spinning; dimethylsulfoxide; forced swimming test; entorhinal cortex; open field; n-acetyl-aspartate; A 1R; paired-pulse low-frequency stimulation; 8-cyclopentyl-1,3-dipropylxanthine; high sucrose; field excitatory postsynaptic potentials; type-2 diabetes; temporoammonic; long-term depression; novel object recognition; γ-aminobutyric acid; object displacement; long-term potentiation