RESUMEN
Spinal Cord Injury (SCI) is a significant neurological disorder that can result in severe motor and cognitive impairments. Neuronal regeneration and functional recovery are critical aspects of SCI treatment, with calcium signaling being a crucial indicator of neuronal excitability. In this study, we utilized a murine model to investigate the effects of targeted wireless electrical stimulation (ES) on neuronal activity following SCI. After establishing a complete SCI model in normal mice, flexible electrodes were implanted, and targeted wireless ES was administered to the injury site. We employed fiber-optic photometric in vivo calcium imaging to monitor calcium signals in pyramidal neurons within the CA3 region of the hippocampus and the M1 region of the primary motor cortex. The experimental results demonstrated a significant reduction in calcium signals in CA3 and M1 pyramidal neurons following SCI (reduced by 76 % and 59 %, in peak respectively). However, the application of targeted wireless ES led to a marked increase in calcium signals in these neurons (increased by 118 % and 69 %, in peak respectively), indicating a recovery of calcium activity. These observations suggest that wireless ES has a positive modulatory effect on the excitability of pyramidal neurons post-SCI. Understanding these mechanisms is crucial for developing therapeutic strategies aimed at enhancing neuronal recovery and functional restoration following spinal cord injuries.
RESUMEN
During the process of seizures, the addition of low-frequency magnetic fields has been proved to be an effective method to suppress epileptic discharges. However, whether adding magnetic fields before the appearance of epileptic discharges can produce this inhibition has not been studied. In the present study, we first constructed epilepsy models on brain slices by perfusing them with Mg2+-free artificial cerebrospinal fluid (aCSF). The events of seizures evolved from inter-ictal epileptiform discharges (IIDs) to inter-epileptiform discharges (IDs). Combined with the multi-electrode array platform, we designed a flexible moving coil to generate a 0.5 Hz magnetic field on the brain slices. Using this method, we added the magnetic fields to brain slices for 30 min before epileptiform discharges were induced. The experimental results demonstrated that although the priming magnetic fields could not completely inhibit epileptiform discharges, they can significantly reduce the frequency of IDs and increase the frequency of IIDs in the CA3 region of the hippocampal slices. In the control group, the rates of IDs and IIDs were 0.0024 ± 0.0006 Hz and 0.0138 ± 0.0043 Hz, respectively, while in the magnetic stimulation group, the rates were 0.0012 ± 0.0004 Hz and 0.0251 ± 0.0067 Hz. Moreover, the results indicated that changing the frequency of interictal discharges did not affect ictogenesis. The results demonstrated that the priming magnetic fields had a certain weakening effect on the frequency of IDs, which was achieved by reducing the signal propagation speed and increasing the excitability threshold of hippocampal neurons.