Abstract

Transcranial light emitting diode therapy (LED) is an energy therapy that delivers photons to the brain by passing through the scalp and skull, being effective in the treatment of some neurological disorders. It is also very attractive because it is a relatively cheap, non- invasive and safe way to modulate neuronal processes by light energy absorption. Here, we evaluated the effect of LED in a murine model of the Alzheimer disease on paired pulse facilitation (PPF), input/output (I/O) and long-term depression (LTD), a type of synaptic plasticity involved in learning and memory. We used hippocampal slices from C57BL/6 (WT) and APPswel/PSNE1DE9 (ALZ) mice (nine-month-old) without LED comparing them with mice that received the therapy (WT-LED) or (ALZ-LED), respectively. LED consisted in the exposition to red light (630 nm) during 125 s for 5 consecutive days. Field excitatory postsynaptic potentials (fEPSPs) were evoked by electrophysiological stimulation in Schaffer collateral fibers and extracellularly recorded in the Stratum radiatum of the CA1 region of the hippocampus. To measure PPF, two pulses were applied at different interstimulus intervals (20, 50, 100, 150, 200, and 250 ms). For I/O, the relationship between gradual increase in the stimulus intensity represented by the amplitude of the fiber voley and the EPSPs slope, were evaluated. LTD was performed by low frequency stimulation (900 pulse at 1 Hz). Our results showed that PPF and I/O did not change between animals with or without therapy. Interestingly, ALZ (n=4) compared to WT (n=6) exhibited abnormal LTD, while that ALZ-LED significantly reversed this effect (n = 7) without affecting the LTD in WT-LED (n = 7; p<0.05; ANOVA one-way test).